The Material Gene: Gender, Race, and Heredity after the Human Genome Project 9780814744727

Citation preview

The Material Gene

Biopolitics: Medicine, Technoscience, and Health in the 21st Century General Editors: Monica J. Casper and Lisa Jean Moore Missing Bodies: The Politics of Visibility Monica J. Casper and Lisa Jean Moore

Biopolitics: An Advanced Introduction Thomas Lemke

Against Health: How Health Became the New Morality Edited by Jonathan M. Metzl and Anna Kirkland

The Material Gene: Gender, Race, and Heredity after the Human Genome Project Kelly E. Happe

Is Breast Best? Taking on the Breastfeeding Experts and the New High Stakes of Motherhood Joan B. Wolf

The Material Gene Gender, Race, and Heredity after the Human Genome Project

Kelly E. Happe

a NEW YORK UNIVERSIT Y PRESS New York and London

NEW YORK UNIVERSITY PRESS New York and London www.nyupress.org © 2013 by New York University All rights reserved References to Internet Websites (URLs) were accurate at the time of writing. Neither the author nor New York University Press is responsible for URLs that may have expired or changed since the manuscript was prepared. Library of Congress Cataloging-in-Publication Data Happe, Kelly E. The material gene : gender, race, and heredity after the human genome project / Kelly E. Happe. pages cm Includes bibliographical references and index. ISBN 978-0-8147-9067-0 (hardback) ISBN 978-0-8147-9068-7 (paperback) 1. Genomics—Social aspects. 2. Human genetics—Social aspects. 3. Genetic engineering—Moral and ethical aspects. I. Title. QH438.7.H37 2013 572.8’6—dc23 2012048186 New York University Press books are printed on acid-free paper, and their binding materials are chosen for strength and durability. We strive to use environmentally responsible suppliers and materials to the greatest extent possible in publishing our books. Manufactured in the United States of America 10 9 8 7 6 5 4 3 2 1

Dedicated to the memory of Elizabeth Chase Lewis (1919–2003)

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Contents

Acknowledgments Preface 1 Ideology and the New Rhetoric of Genomics

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2 Heredity as Ideology: Situating Genomics Historically

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3 Genomics and the Reproductive Body

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4 Genomics and the Racial Body

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5 Genomics and the Polluted Body

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6 Toward a Biosociality without Genes

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Notes Bibliography Index About the Author

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Acknowledgments

I count myself lucky that this book was mostly a labor of love and not just, well, labor. I have many people to thank for that. First, I’d like to thank Carol Stabile for many years of mentoring, support, and friendship. Her work on the intersection of feminism, technology, and political economy proved absolutely crucial to my thinking. I continue to reap the benefits of the top-notch education I received at the University of Pittsburgh. Many thanks go to John Lyne, Gordon Mitchell, Robert Olby, Peter Machamer, John McGuire, and Danae Clark. In the ensuing years, I have benefited from colleagues and mentors who invested their time and energy in my intellectual and scholarly growth. I thank Karen Whedbee (especially for proving that the intellectual is not an endangered species in academia after all), Rob Brookey, Lois Self, and Beatrix Hoffman for much-appreciated feedback and support. At the University of Georgia, I thank Chris Cuomo, Patricia Richards, Susan Thomas, Bethany Moreton, Juanita Johnson-Bailey, Tom Lessl, and Roger Stahl for their inspiring scholarship and for their generosity in supporting my own work. Ed Panetta, my colleague in the Department of Communication Studies, was my intercollegiate debate coach many moons ago— I’m not at all surprised that I appreciate him as a colleague as much as I appreciated him as a mentor during those formative undergraduate days. Barb Biesecker has introduced me to both biopolitical scholarship and the people producing it—and this book has benefited as a result. Celeste Condit long ago inspired my interest in rhetoric and genetics; more recently, she has been a cherished mentor. I continue to enjoy our conversations about life, work, and, of course, genes. Finally, I thank Darrel Wanzer, Phaedra Pezzullo, Ron Greene, and Stuart Murray for their advice, engaging conversations, and influential scholarship. >>

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and inventing the Prosecco play date; and especially to Patricia Richards for being such a great friend and colleague, demonstrating that it is all worth it in the end, and most importantly, for agreeing with me a lot. I am especially lucky for my given family, which includes Jeff Happe, who helped with the transition back to Athens (and who, along with Molly Happe, introduced me to leftist politics at an early age); Pam Adriance, who made much-needed family time possible; and Brooke Ryan, who is the best auntie Dash could ever hope to have. My godmother, Cheryl Patrie, has been generous and kind and remains one of my biggest cheerleaders. The entire Barnard clan warmly welcomed me into their family with much holiday time respite and good cheer. “It takes a village,” they say, and I’ve had quite a nice one in Athens. I’d like to thank, from the bottom of my heart, the following people, who loved my son as if he were their own: John and Dana Butler, Gloria Huesser, Chelsea Woods, Madie Fischetti (of the infamous “Fischetti Five”), Elizabeth Hargrove, Patricia Richards, Oscar Chamosa, and, of course, my mother, the enormously talented Karen Lewis, whose generosity seemingly knows no bounds. She repeatedly made the long drive to Georgia to shower Dash with gifts, kisses, and cake, and she continues to model what it is to be a strong, intelligent, and principled woman. I thank my partner, Clark Henderson, for love and companionship. His bravery in the face of some of life’s most cruel challenges has been an inspiration. His thirst for knowledge, brilliant mind, and unshakable moral compass both challenge and ground me. Plus, he’s fun to hang out with. To close, I thank my sweet cherub of a son, Dashiell, whose attitude toward life is something along the lines of “Why walk, when you can skip?” You came into my life when I needed you most.

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Preface

On January 11, 2008, I lost my good friend Chet Meeks to colon cancer. Chet was, without a doubt, one of the smartest, most talented scholars I’ve had the good fortune to know. I learned a great deal from him over the years. Chet was just thirty-two when his cancer was first diagnosed; he died two years later. Chet did not lead an unhealthy lifestyle. He was not genetically predisposed to colon cancer. No one in his family had been diagnosed with colon cancer. The etiology of Chet’s cancer was, and will remain, a mystery, although he often wondered about the years he spent living near the Hudson River, polluted with polychlorinated biphenyls (PCBs), when he was pursuing his PhD in sociology. Determining ultimate causes is not, understandably, high on the list of one’s concerns when diagnosed with cancer. Chet’s goal was treating the cancer and curing it despite considerably bad odds. For the cancer patient, little emotional or intellectual space exists for theorizing one’s disease in the midst of learning about the medical array of tests, treatments, and “cures.” Nevertheless, I know that Chet was, on some level, encouraged by the work I had been doing on genomics, epidemiology, and the politics of cancer, keeping conceptual and critical questions on the table, holding onto the necessity of theory in the midst of crisis—of real, in-your-face, material exigency. He was, after all, a social theorist. Although theory can be abstract, it is also an indispensable tool for making sense of the varied and often contradictory details of individual and collective embodied experience and everyday life. As Paula Treichler reminds us, “theory is not the creature disdained by  .  .  . anti-intellectual traditions, including U.S. medicine, for whom theory is defined as that which is devoid of relevance >>

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medicine predicts a future of what is called personalized medicine, wherein a patient’s genome becomes the site of diagnosis and treatment of risk. On the other hand, hereditarian thinking imagines patients racially, which means that personalized medicine has the potential to become yet another privilege of white patients, for whom race does not enter into diagnosis and treatment practices. Despite the paradox whereby genomics simultaneously reifies both individuals and populations, its immanent hereditarianism nevertheless effects a crucial displacement in both cases: disease is evidence of inherited defects, not embodied life. Genomics is, then, more than a disease paradigm—it is a political worldview that has been both a constant in US history and a particular way of performing ideological work during discrete moments in that history. Indeed, my interest in genomics began long ago with the question, what makes the genomic model of disease distinct from other models? The answer to that question emerged largely through a particular reading of eugenics. During a regrettable period of history in which a vicious racism and nativism intersected, however tangentially, with the newly discovered theory of heredity, eugenics justified—in the minds of reactionaries and progressives alike—the figurative and literal criminalization of blacks, women, immigrants, and poor people. Why, I ask in this book, has heredity remained uniquely suited to the task of constructing biopolitical discourse during crucial and sometimes painful phases of industrial capitalism and emerging social movements and discourses of resistance? To understand why it matters that Chet was stricken with an aggressive cancer at such a young age, we must think beyond his individual body and the treatments it required. We must think of his experience through the framework of collectivity: of his body located in space and time with others, living in environments and social relations not of their own making but resulting from deeply politicized and self-interested corporate, governmental, and institutional practices. To answer the questions I pose requires the humanist’s eye, located a safe and critical distance from the disciplinary norms of genomics, medicine, and public health. In the spirit of scholarly inquiry, and in memory of Chet’s unrivaled intellect and sense of humor, I present the following study.

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1 Ideology and the New Rhetoric of Genomics

In a 1999 article in the journal Plastic and Reconstructive Surgery, a surgical team describes the case of “A.H.,” a patient who undergoes an elevenhour operation to remove her breasts, ovaries, and uterus. The surgery also included the reconstruction of breasts using skin and tissue from various parts of her body. In all, the surgery involved three separate surgical teams and was divided into four stages. After a four-day hospital stay, A.H. was released; she underwent additional procedures on her breasts over the next seven months. Although narrated in the matter-of-fact clinical language of the case report, the surgery was, in fact, radical, even gruesome, and the article included photographs of her body from the neck down with the customary markings of the plastic surgeon, noting the location of various incisions and cuts necessary to refashion her physique. Such surgery requires, the report informs us, “significant recovery time.”1 The authors of the report predict that the procedure will extend the life of A.H. by four to six years “or more,” even though the decision model they employ assumes that there is a complete mastectomy and no reconstruction (which in fact A.H. had), and that the patient tolerates, and complies with treatment during many years of potentially dangerous hormone replacement therapy. What sort of disease would necessitate such interventions? As it turns out, no disease at all, at least not in the conventional sense of the term. A.H. did not have cancer, nor did she have any symptoms of diseases related to the reproductive organs. The surgery was attributed, rather, to a positive test for a mutation of one of the so-called “BRCA” genes—in this case, a mutation of BRCA2.2 Inheriting a mutation of one of these genes increases a woman’s risk for breast and ovarian cancer. A.H.’s surgery was performed for the sole purpose of reducing her risk for both. Many >>

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culturally inscribed—Katherine Hayles calls this the outcome of ideological transcription practices4—genomics is dependent on normative conceptions of the gendered, raced, and bounded body. As Catherine Waldby reminds us, “Biomedical knowledge cannot . . . be quarantined from general ideas operative in the culture, even when it understands its concepts to be carefully and directly deduced from the factual evidence of the body. Despite, or perhaps because of, biomedicine’s assertion of its own innocence of historical and political meaning, it constantly absorbs, translates and recirculates ‘non-scientific’ ideas—ideas about sexuality, about social order, about culture—in its technical discourses.”5 Not only must genomics rely on cultural discourses about the body to translate genetic information into body practices, but in doing so it will in turn participate in their construction. It thus contributes to our shared meanings of race, gender, and embodied life. Indeed, the very conditions of intelligibility on which the story of A.H. depends in both popular and scholarly discourse rest on hidden, and heretofore underexamined, assumptions about gender, race, and political economy. Family history aside, A.H., through the visualization and objectification of her body, is removed from any context that might allow for a consideration of why the female medical subject figures so prominently in the genomics revolution; how gender and race determine whether the removal of her organs is the rational way to prevent cancer; whether her genomic profile is simultaneously a racialized one; and whether the risk she fears is appropriately construed as an inborn trait. We must interrogate these otherwise mystified embodied materialities to understand not only how the normative body mediates the translation of inherited risk into actual biomedical practices, but also how biomedical theories and the social and economic order inform each other. The chapters that follow thus recontextualize the body of A.H. and theorize its materiality within a cultural, economic, and political context. In so doing, the book explores genomics’ implicit investment in the very norms and values on which its translation into medicine and public health depend. A central argument of the book is that explicit ideological appeals are no longer required for genomics, and biomedicine more broadly, to shore up the values of the free market, the racism of biological types, and the antifeminism of the conflation of gender and sex. Rather, the means by which genomics performs this ideological work (and, indeed, how it serves its own institutional interests) has along with shifts in gender and racial politics, social movements, and political economy. I attempt to

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explain—that necessitates its figuring in any critical account of genetics today. As I will show throughout the book, genetics never abandoned its investment in the normalization of bodies and the larger social and economic order, even as it set out to reinvent itself after the demise of the eugenics movement. However, since genomics is no longer articulated to explicit political projects like eugenics and its close cousin social Darwinism, we must consider how hereditarian ideology is located in what Sandra Harding, following Fredric Jameson, calls science’s “political unconscious.”6 For Harding, science’s cognitive core—the collection of theories, models, tools, and norms that guide its practices—is never merely that. Rather, embedded within those practices is a politics, an investment in a particular arrangement of social relations outside the confines of the research setting. Responding to what she says is the myth that “inegalitarian political projects remain external to fundamentally value-free scientific assumptions, methods, and claims,” she argues that science is always already ideological, even when it passes the highest standards of methodological excellence and explicitly distances itself from culture, politics, and political economy.7 A closely related concept is Sheila Jasanoff ’s notion of “co-production,” a novel take on knowledge making in scientific research that “calls attention to the social dimensions of cognitive commitments and understandings, while at the same time underscoring the epistemic and material correlates of social formations.”8 Thus science is also a form of social knowledge,9 but with a set of epistemological practices and discourses unique to it. The concepts “political unconscious” and “co-production” together capture the complex relationship that institutions have with each other and with the social and economic order.10 These relations are not always direct or easily mapped. Instead, they manifest themselves as a form of ontological or ideological complicity—separate fields of discourse that are semi-autonomous (and so are characterized by epistemological practices unique to them), but nevertheless permeable to and thereby shaped by historically resilient dominant interests and their cultural logics.11 Throughout the book I show how, through an institutional discourse of health and healing, the political unconscious of genomics—its hereditarianism—has become more difficult to locate and map but nevertheless remains a powerful method for naturalizing social and economic relations. Human genetics’ insinuation into the provinces of medicine and public health has been one of the most effective means by which it claims to be free of such interests. Having retreated to the world of the laboratory after

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overdetermines meanings of the gene, even in those models that purport to give due consideration to the agency of environmental contexts. The synchronic view, in contrast, holds that gender and race are descriptors of lived and embodied experience, and as such are inextricably bound with political, social, and economic structures.16 A synchronic view of race, for example, would require an examination of social isolation, geography, and what critical race scholars call “microaggression”—the relentless exposure to small acts of racial prejudice on an everyday basis.17 And it would treat these variables as historically contingent, materializing in ways particular to a given place and time. What does it mean, for example, to embody racial identity in a specific geographic location, during a particular stage of capitalism, and within historically specific practices of institutional racism? And with these questions in mind, what does it mean to embody sex? These different models of the body and disease matter not only because of the kinds of biomedical practices they call forth (what science studies scholars have called the inextricable link between representing and intervening)18 but also because describing bodily attributes in synchronic terms makes possible a particular kind of agency and accountability— namely, a call for changes in economic and social policy as a way to effectively deal with health inequities. Genomics’ privileging of the diachronic over the synchronic thus reveals a logical homology between its practices and the political discourses that rely on such a displacement. As Jasanoff says of “co-production,” the “ways in which we know and represent the world (both nature and society) are inseparable from the ways in which we choose to live in it.”19 Genomics is by no means alone in privileging a diachronic reading of the body and disease—I will show that, in many ways, it has acted as the successor to epidemiological discourse that has trafficked in the idea that the body can be broken down into proximate, isolatable, and static components. Indeed, biopolitics scholars have quite persuasively questioned the very notion of health. Genomics has not, however, enabled the types of progressive discourses that epidemiology has.20 Heredity, I will suggest, is overdetermined by its eugenics legacy—a cultural logic that translates the pathologies of economic and social relations into pathologies of bodies—inherited at birth and immune to change.21 The chapters of the book together examine how this logic is introduced and what is at stake by asking: How do genomics and its implicit hereditarianism enter into long-standing debates about women, reproduction, and the ideology of

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space wherein the historical, material, and contingent conditions of capitalism are visualized, and eventually internalized, as the natural order of things?25 Donald Lowe, in The Body in Late-Capitalist USA, says that bodily practices reflect the changing needs of the market and are ways in which its values become part of common-sense, everyday, embodied life. For example, deskilling changes the material ways in which the body produces surplus value, by radically constricting and accelerating one’s movements; sexuality and gender become commodifiable “lifestyles.”26 By drawing from both Marxist and discourse methodologies, Lowe compellingly shows the advantages of a synchronic analysis of the body: bodily practices are enabled by specific configurations of discourse and of production and consumption practices, the latter being unique to the stage of capitalism in which the analysis proceeds. But the circulation and imposition of these values will not affect all bodies in the same way. As Waldby observed in her study of AIDS discourse, body practices are a mechanism for the enforcement of social norms. Thus, we must attend to the specific ways in which systems of gender and racial oppression are called on to discipline bodies.27 In this way, racism and sexism are understood as social phenomena distinct from economic structures and relations (and so not reducible to them), but nevertheless integral to their successful operation.28 Regarding race, Lowe writes that its context “cannot be analyzed in terms of an orthodox Marxist structural order, but as a hegemonic terrain of exchangist practices, with the recombination of structural, discursive, systematic, and semiotic components. And the very structural, discursive, systematic, and semiotic components are premised on the pervasiveness of racism. In other words, race operates within a hegemonic terrain, and that terrain takes advantage of existing racism. In reality, the two are intertwined.” Race is “neither a monolith, nor an isolatable variable,” he continues. “Therefore, let us abandon the search for an isolatable racism which, in effect, frees all other variables from any responsibility,” for economic interests are often secured by exploiting “existing racial stratification and racism.”29 Lowe’s analysis, in providing a synchronic account of bodily practices during the mid-1990s, both shows us how the body is the site for the production of surplus value and, in so doing, also shows us how body scholarship can help explain particular stages of capitalism. In this book, I too want to look at the lived body in late capitalism (or, more precisely, neoliberalism), but not as a way to understand the body as a site for capital accumulation per se (that work has been done already).30 Rather, taking

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As with [sickle cell anemia], so more generally in the relations between race and genetics: these links have no given or intrinsic politics; they take very different forms as they are entwined with distinct styles of thought about health, illness, and the body at different times and places. And, as with [sickle cell], the relation between these terms today, in the United States at least, is intrinsically linked to the delineation and administration of biosocial communities, formed around beliefs in a shared disease heritage, demanding resources for the biomedical research that might reveal the genomic bases of these diseases, and mobilized by the hope of a cure. Perhaps, then, we might understand the contemporary allure of race in biomedicine in terms of the hopes, demands, and expectations of such communities of identity, as both subjects and targets of a new configuration of power around illness and its treatment.31

There is little doubt that the allure of race is indeed a product of the collective demand of various communities of persons that biomedicine attend to, among other things, disparities in the incidence and death rates of various diseases. The problem with Rose’s overall argument, however, is that he mistakes the desire for a progressive genomics with the possibilities for one. Put another way, inclusivity does not necessarily entail a corresponding shift in political or ideological alignments. The constellation of varied agendas is not, I would argue, evidence that the science itself, and its technological interventions, are value-free, undetermined by the conditions of their emergence.32 Certainly, genomics’ attention to race may appear to satisfy many interests simultaneously, especially those of African American members of the medical and research communities. Yet this convergence can coexist with an otherwise undisturbed system of racial oppression.33 And this system of oppression, as well as others, becomes more difficult to discern. Carol Stabile, in her work on the intersection of feminism, technology, and political economy, has argued that dominant interests can accommodate and withstand apparent challenges to their hegemony.34 In fact, they often must adapt to new material and discursive conditions, and this adaptation does not always require recourse to older ideological scripts. Ideological contradictions, she writes, are not necessarily resolved in favor of “tradition,” but resolve or repress “ideological contradictions through a logic of progression.”35 Perhaps nowhere is this more apparent than in the field of medicine, which earlier in its history very explicitly

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fields of power-charged differences, not essences and natural origins or homes. Race and sex, like individuals, are artifacts sustained or undermined by the discursive nexus of knowledge and power. Any objects or persons can be reasonably thought of in terms of disassembly and reassembly; no ‘natural’ architectures constrain system design.”40 Likewise, developments external to genomics—such as the social changes brought about by civil rights, feminist, and environmental movements—have compelled significant discursive shifts. Gynecological oncologists are careful to qualify treatment recommendations that may conflict with the reproductive autonomy of women, a development that reflects the influence of the women’s health movement. Moreover, opposition to ovary removal is not likely to be based on the notion that it “desexes” or “defeminizes” women, a reflection of the success of feminism in disarticulating sex from gender identity. Manipulating the body at risk can be reasonably interpreted as a way to distance oneself from a naturalized, inviolable understanding of female sexual identity. The postgenomics body becomes a cyborg of sorts: one with prosthetic breasts and chemical hormone supplements; and one that embodies flexible, contingent notions of environmental risk. The emergence of influential women’s and African American health movements, moreover, has meant that all fields of biomedicine, including genomics, feel a responsibility to attend to the health disparities that continue to befuddle epidemiologists. In many ways, developments in biomedicine—and genomics, more specifically—are seen as welcome changes to medicine’s historical unwillingness to address gender and racial disparities, a failure that has contributed to social inequalities between women and men and between blacks and whites. And finally, a growing awareness of the links between environmental pollution and disease has given new importance to the gene-environmental model of disease etiology. Environmental breast cancer activists, for example, have repeatedly called on researchers to investigate the complex origins of tumors, including the role of genes in increasing one’s susceptibility to toxic chemicals. These discourses, still unfolding, have produced bodies seemingly devoid of genetic or cultural essences but that nevertheless require continued study and care. This logic of progression pervades much of the discourse of genomics: genetic testing can save women’s lives; gene-environment interaction is a model for improving public health, not just the health of those with rare genetic disorders; and the genome provides material evidence of the

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prediscursive, value-free materiality. Constituted by culture and dominant beliefs about race, sex, and sexuality, bodies in turn exert influence on the scientific discourses about them. Says Harding: “Scientific practices inevitably must ‘deliver’ nature to us in an already discursively encultured form.”44 This is especially the case in genomic medicine, in which the researcher’s gaze shifts from the molecular to the somatic in an attempt to translate the products of genetic tests into cancer prevention. Scientific practices, then, will be shaped by—and will, in turn, shape—enculturated, normative bodies.45 This interplay between discourse and inscribed material objects is what the philosopher Karen Barad calls the performative understanding of scientific practices.46 Discourse, then, is where habits of mind are reproduced, far removed from the intent or consciousness of its authors or from the material practices of the laboratory. More important, however, discourses traverse institutions and the larger social and economic structures of which they are part. Science may appear institutionally distinct from the larger culture, given the norms of objectivity and accompanying sanitized lexicon that are peculiar to it, yet because it is an institution, it comprises persons whose positionalities reflect an investment in certain class, race, and gendered relations. Specific disciplines, for instance, may have their own way of defining race, but it is nevertheless the case that certain hegemonic meanings of the term (that is, race as a biological artifact) emerge across the boundaries that define and otherwise separate them. A rhetorical perspective attends not only to shared beliefs across mulitiple discourses but also to the inner workings of the texts that form them. How, for example, do certain meanings of the gene emerge? Or meanings of ovaries? Race? Risk? Put another way, how do objects become objects? In the field of science and technology studies, Jasanoff describes this as “the emergence and stabilization of new objects or phenomena: how people recognize them, name them, investigate them, and assign meaning to them; and how they mark them off from other existing entities, creating new languages in which to speak of them and new ways of visually representing them.”47 What Jasanoff captures in this passage is the way in which a rhetorical approach to scientific practices opens up space for considering change, but not in terms of a positivist history of science, replete with origins, linear unfolding of ideas, and presumptions regarding the ontological status of objects.48 Rather, scientific practices—the conjunction of theories (and their assumptions about the material world), instruments, and observers—collectively enable the emergence of an object of study.

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concept of race as a biological construct is scientifically invalid, it is also tenacious—embedded in institutions and habits of language. It serves manifold interests in maintaining the status quo, from which science is hardly separate. A rhetorical analysis of genomics discourse shows that— despite the recalcitrance of the genetically diverse body that critics of race would say is a material reality that simply cannot be outmaneuvered by racialists—a racially coded body nevertheless persists, not in spite of the existence of genetic diversity, but in many ways because of it. My analysis shows, in fact, that relative genetic diversity now serves as the way geneticists can distinguish African Americans from other racial and ethnic groups. Genetic diversity, then, serves the interests of antiracialists and neoracialists alike. The case of race thus shows the benefit of a rhetorical method that takes cultural studies’ notion of hegemony as a starting point, insofar as discourse is the means by which dominant ideas are both circulated as common sense and shared among otherwise contrary interests. However, the language of these ideas is rarely, if ever, “the language of the rulers.”53 In the cases I examine, it is the language of science. This is the benefit of the rhetorician’s unique ability to identify the relevant, enabling conditions of a specific institutional discourse (its material exigencies and constraints) in conjunction with its inner workings—the particular tropes, arguments, and linguistic arrangements expressed as scientific paradigms and experimental norms, together constituting its meaning-making practices. Before I review the book’s chapters, I must first explain its African American focus. I have already described the difference between understanding race as lived experience and defining it as a biological state. I have also looked at this distinction, drawing on Stevens, according to the difference between a synchronic and diachronic understanding of race. Doing so helps us understand more clearly several phenomena in genomics research and the application of that research in clinical medicine. These are the construction of the medical subject, specifically the intersection of gender and race in surgical guidelines for oophorectomy (requiring an analysis of reproductive justice issues specific to African American women); the redefinition of disease from a product of racism to a product of evolutionary history; and the similar transfer of causal power from industrialization to genes in the field of environmental genomics. In all of these cases (the topics of chapters 3, 4, and 5, respectively), I proceed on the assumption that in order to attend to what is at stake in genomics’ incursion into medicine and public health, we need both an examination

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feminists in disarticulating the body from reproduction creates a space wherein it is thinkable to remove ovaries and breasts. The implicit assumption in genomics discourse is that to deny life-saving operations is to necessarily embrace an identity rooted in the normatively gendered body (as when preserving ovaries or breasts on the grounds that they are essential to feminine, sexual identity). Paradoxically, the conditions for the organs’ removal are structured by traditional ideas of reproduction and motherhood: ovaries can be conserved, but only for a time, and only to answer to the desires of young motherhood. In contrast to those of white women, black women’s ovaries are treated very differently: too often left in the body when cancerous, too easily removed to appease implicitly racist (and fabricated) anxieties over race and reproduction. And whereas young pregnancy and multiple pregnancies are permitted, even encouraged, in BRCA discourse (young pregnancy decreases cancer risk and fulfills procreative desires before genetic fate takes over), pregnancy has emerged in the cancer literature as a cancer risk for black women. Once again, black pregnancy is a pathological condition, a discursive development that must be read against the backdrop of a long-standing discourse in the United States linking black women, reproduction, and poverty. In contrast to chapter 3, in which the BRCA subject is racially unmarked (thus masking white privilege), chapter 4 considers the context in which the BRCA subject is racially marked, that being the population turn in genomics research on breast cancer. The initial goal of BRCA sequencing may have been to serve the needs of women in what are called cancer syndrome families—those 5 to 10 percent of women with breast cancer whose disease is thought to be due to inherited genetic susceptibility—but it wasn’t long before the prospect of wider applicability piqued the interests of researchers. Such a breakthrough occurred in 1995 with the description of three BRCA mutations found in women who were not related. It was simultaneously an “ethnic” turn, as the women with these three mutations all identified themselves as members of the Ashkenazim. With this development came the prospect that BRCA research (and in particular the BRCA test) would be relevant to a much larger group of American women: those connected through evolution, but genetically isolated through culture. Two years later, researchers published data gleaned from a study of African American women with breast cancer.57 Chapter 4 argues that the population turn has simultaneously been a racial one. This is perhaps not surprising, since racial thinking was never fully rejected by the biomedical community, often operating surreptitiously under the

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can rationalize environmental health interventions by identifying those who are truly at risk. Identifying and classifying persons at varying levels of hereditary susceptibility is not, however, progress as much as it is simply a different, albeit also value-laden, way of describing bodies, environments, and social relations. The discourse of environmental genomics presumes the individual to be the site of environmental health intervention—and only certain individuals at that. Two aspects of this discourse are particularly pertinent to my argument. First is the presumption that it is irrational, from a cost-benefit perspective, to regulate environmental pollutants without knowledge of individual genetic susceptibility, the implication of which is that current pro-industry regulations should remain largely unchanged. Second is the construction of a neoliberal subject of environmental genomics, through which behavior modification is seen as the common-sense course of action in response to toxic environmental exposures. The entrepreneurial consumer of new technologies and therapeutics becomes the agent moderating the impact of environmental exposures, thus leaving the market largely in control of what those exposures will be. This chapter ends with a gesture toward a different type of body politics, one grounded in embodied experience and social movement. In the book’s conclusion, I extend this discussion by arguing for a postgenomics ethos, what I call a biosociality without genes.

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2 Heredity as Ideology Situating Genomics Historically

Two years ago I attended a panel discussion on epigenetics, part of the University of Georgia’s “Darwin Days” series of events. I was interested in the panel because epigenetics exemplifies for me the stunning creativity and innovation of modern-day genomics research. Not surprisingly, Lamarckism came up—in particular, its association with Soviet-era genetics research, most of which was based on the materialist notion that environmentally induced changes could be transmitted to one’s offspring. One of the panelists eventually proclaimed, “Well, I guess we’re all Marxists now!” I took this comment to be an implicit recognition (even in its attempt at humor) that theories of gene-environment interaction are deeply political. Yet despite the potential of gene-environment research to rethink the nature-nurture debate, in practice and in language it seems as though it is nature that always triumphs.1 Even with the revelation announced not long before this book went to press that “junk” DNA, as it turns out, is no such thing, and may be even more important than genes, the genome remains central. In some ways, even epigenetics does not move us far afield from the centrality of heredity, as only those environmentally induced changes that can be inherited and that violate the implicit sanctity of the genome will be the drivers of research. Indeed, it is hard to fathom what sort of genetics research could displace the role that heredity firmly holds in the wake of the HGP and its extensive fanfare.2 What might be called an ontological complicity between genomics and the economic and social order has been a historical constant, even if its particular configurations have changed. It is essential to shed light on this complicity so as to correct for the mistaken belief that contemporary genomics bears no traces of the kind of thinking that informed earlier >>

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interest in Gregor Mendel’s pea studies in 1900, the American eugenics movement was most active between 1900 and 1930.3 Following popular family studies such as The Jukes,4 Charles Davenport, a researcher at Cold Spring Harbor Laboratory5 and one of the best-known American eugenicists, opened the Eugenics Record Office (ERO) in 1906 with funds from the family of the railroad magnate E. H. Harriman. The purpose of the ERO was to study the link between heredity and human behavior.6 The American Eugenics Society was formed in 1923 and soon included twenty-eight state committees and a branch in southern California.7 Eugenicists such as Davenport believed that heredity explained phenomena like class, intelligence, criminal behavior, and disease—all problems perceived to be particularly acute at the beginning of the twentieth century. To provide support for the heredity theory, the ERO logged information gathered by its fieldworkers from house surveys, prison and hospital records, almshouses, and institutions for the deaf and blind as well as those classified as “mentally deficient” and “insane.”8 Davenport and his fellow eugenicists argued that the information they gathered demonstrated a link between biology and the pathological behavior they observed in the field. For advocates of positive eugenics—the idea that genetically superior people should be encouraged to breed in order to propagate the best traits—ERO data were essential in making decisions about marriage and having children. Mendelism demonstrated that many traits were recessive and, if applied to human behavior, meant that family histories were essential to determine the chances of breeding those termed “undesirables.” The “better baby contests” held throughout the United States are an example of the ways families were formally recognized for their enlightened breeding practices. The notion of positive eugenics arguably explains why many progressives were also eugenicists,9 in that they saw better breeding as an enlightened supplement to social welfare: The American [progressive] movement was in large part the creation of superintendents of asylums for the feebleminded, insane, and alcoholic, of prison wardens and prison physicians, of sociologists and social workers. They were in the forefront of the movement for bigger and better institutions to house and treat the unfortunate classes of mankind. They believed that society had a responsibility to care for the dependent and delinquent but that society had, at the same time, a responsibility to see that such persons did not contaminate the generations to come.

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What was at stake in the nature-nurture debate of the 1920s was no less than civilization itself—a rhetorical shift that characterized the backlash of the decade. Wiggam elaborated in mid-decade: Charity, hygiene, sanitation, and the triumphs of chemical, biological, and medical genius have preserved for reproduction great numbers of incompetents and defectives who in the good old days of natural selection would have died young. Civilization is thus seen to be a selfdestructive enterprise, the most dangerous enterprise upon which mortals ever set out, and one which, by its very nature and objective, sets going those agencies which in the end destroy the men that built it and insures its own dissolution.15

Circulating this discourse of “race” suicide, eugenicists successfully lobbied for some of the most reactionary legislation in US history. In 1924 the Immigration Act was passed by overwhelming majorities in both the House and the Senate and was signed by President Calvin Coolidge. For the next three years, immigration was limited to a small percentage of those nationalities recorded in the 1890 census, in an effort to target the Eastern and Southern Europeans blamed for race deterioration and social unrest (since there were far fewer Eastern and Southern Europeans in the United States in 1890, the immigration restriction affected them most severely). And in 1927 the Supreme Court upheld the legality of some twenty state sterilization laws in Buck v. Bell.16 Stakeholders in contemporary debates about genetics point to the eugenics movement as evidence of the power of genes to justify extreme, misguided discrimination. Yet it is also important to consider the extent to which eugenics included an unstated politics that was palatable to diverse audiences. As I pointed out above, many eugenicists were progressives, illustrating the appeal of scientism for professionals who saw themselves as the experts most able to address the effects of industrial expansion. In fact, the middle class provided the bulk of support for the eugenicist cause. The membership in the American Eugenics Society never exceeded 1,200 members, but the middle class was well represented. The movement’s leaders belonged to the professional class, including physicians, social workers, clerics, writers, and professors in the biological and social sciences.17 And although the group’s membership was small, eugenic theories reached large audiences. The ERO devised many methods for disseminating its research to a largely middle-class audience. According

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initiative.”22 To be practical and independent meant studying and living by the laws of heredity, not subscribing to any particular ideology, on the Left or the Right. Lothrop Stoddard wrote in Revolt against Civilization, a eugenicist tract, that Bolshevism violated the natural hereditary order: “Against this formidable adversary stands biology, the champion of the new.”23 Lewis Terman, who led the successful effort to institutionalize intelligence tests, went so far as to suggest that “laborers,” who are not as genetically fit as “managers,” would “drift easily into the ranks of the anti-social or join the army of Bolshevik discontents” if not “trained” properly.24 Indeed, the genes of leftist leaders themselves were called into question: in the proposed immigration restriction legislation of 1914, “revolutionaries” were categorized under “psychopathic constitutional inferiority,” essentially a eugenic category.25 Thus the turn to nature, a turn for which the science of genetics was particularly well suited, came at the expense of questioning, in any meaningful way, the status quo.

Reform Eugenics: Geneticists Retreat to the Laboratory After achieving most of its political successes during the 1920s, the “mainline”26 American eugenics movement experienced a steady decline during the 1930s.27 During this decade, the rise of fascism in Europe and the economic crisis drove many scientists to the Left,28 which arguably accounts for what historians characterize as eugenics’ decline in popularity among the general public. The Third International Congress of Eugenicists, held in New York City in 1932, drew fewer than a hundred attendees.29 By 1940 the ERO, headed at that time by the zealot Harry Laughlin, closed its doors. In an effort to respond to critics, several prominent scientists openly condemned the views of mainline eugenics and articulated what historians have called “reform eugenics.” Reform eugenicists “rejected in varying degrees the social biases of their mainline predecessors yet remained convinced that human improvement would better proceed with—for some, would likely not proceed without—the deployment of genetic knowledge.”30 Specifically, reform eugenicists discarded mainline views concerning race: In the reform-eugenic view, society needed the reproductive contribution of all competent people. Mainline concern with “the race” was beginning to be replaced by attentiveness to “the population.” The new

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Nevertheless, key revenue streams for molecular biology, including research on the transmission of heritable traits and the exact physical structure and chemical composition of genes, bore traces of the eugenics legacy, if only indirectly. Newly formed molecular biology programs drew much of their funding from private foundations that remained keenly interested in the relationship between genetics and human behavior (the term “molecular biology” was in fact first coined in 1938 by Warren Weaver, a Rockefeller Foundation trustee).41 The rising popularity of molecular genetics had much to do with the recognition in the 1930s that eugenics was a liability—it was bound to racist, nativist, and reactionary views and policies, which in turn were based on bad science. Geneticists wished to distance themselves from both. For example, when Morgan publicly attacked eugenicists in 1925 for confusing nature with nurture and ignoring more “enlightened” explanations for human behavior,42 he represented many plant and animal geneticists who distanced their work from both eugenics and the emerging field of human genetics. Many researchers who worked during the 1930s recalled being discouraged from having any association with human genetics on account of its origins in the eugenics movement. As Kevles notes, “indeed, in the United States, plant and animal geneticists tended to discourage prospective colleagues from having anything to do with human genetics, reminding them that it was associated with the racism, sterilizations, and the scientific poppycock of mainline eugenics.”43 The Rockefeller Foundation, an earlier supporter of eugenics, likewise distanced itself from the field in the 1930s, although it never lost interest entirely in the relationships among biology, heredity, and behavior (that is, social pathology). The foundation’s goal in the 1930s was to recuperate the basic science via well-funded interdisciplinary programs, bringing together scholars from a variety of fields and being very careful not to publicly link the basic science to any particular agenda. But, as Lily Kay’s history of the foundation reveals, it envisioned molecular biology as a salvation science, much like its eugenicist predecessors: “The paucity of knowledge about physical mechanisms of gene action represented merely a delay in understanding the basis of intervention; lack of knowledge meant a need for fundamental research. The implicit belief in unit characters,44 even among life scientists, persisted well into the 1940s, along with the intuitive expectations of eugenic intervention.”45 Specifically, the Rockefeller Foundation justified its support of molecular biology on the grounds that it would “rationalize” the human sciences

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could then help promote the breeding of persons who were mentally stable, physically fit, resistant to disease, and in control of their so-called drives.50 Social control was already a dominant paradigm in the human sciences, on which the foundation could draw for its vision for molecular biology: “A little reflection will show that all social problems are ultimately problems of social control—capital and labor, prostitution, taxes, crimes, international relations.”51 The foundation thus put into place an early version of sociobiology, but with an explicit focus on serving the needs of the capitalist order. Molecular biology served this goal by providing the scientific means for producing good, dependable workers (similar to eugenics, molecular biology could easily tie pathologies such as mental illness to political resistance to the economic order). Moreover, the scientific management of human behavior could serve as a justification for scaling back social programs. No more useless funds would be wasted on the unfit. If the political and social culture of the 1930s had brought nurture into the foreground, the Rockefeller Foundation would counter with an intellectual and material investment in nature. The Great Depression had also, according to Kay, sown the seeds of a backlash against scientists and engineers; the excesses and failures of industrial capitalism (now under even more scrutiny because of the fantastic failures of the market) were seen as inextricably tied to the expertise behind their so-called rationality. Thus, the Rockefeller Foundation’s foray into the biological sciences would also help rehabilitate the image of the scientist expert. As in the eugenics era, scientists could once again be seen as enlightened, nonpartisan experts serving the interests of the public good. Indeed, “the launching of the Rockefeller Foundation’s new deal for biology as part of its commitment to the human sciences could not have come at a more auspicious time.”52

The DNA Revolution and Postwar America The molecular biology research supported by the Rockefeller Foundation in the 1940s augmented the field of molecular genetics, with many researchers focusing their investigations on the relationship between the three-dimensional structure of molecules and their functionality.53 For James Watson, Francis Crick, and Rosalind Franklin, the molecule generating the most interest was deoxyribonucleic acid (DNA), shown to be the “agent” of heredity in 1944.54 In April 1953, Watson and Crick published an explanation of just how this agency was exercised (they did not

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molecular biology is not complete without attention to the significant number of physicists who turned their attention to biology, seeking refuge in the “secrets of life” after their stigmatizing association with the “secrets of death.”60 What were the important developments that contributed to the rise of genetics—in particular, of DNA as the agent of heredity—as a culturally significant scientific discourse in the 1950s? One factor was the considerable increase in federal funding for genetics, especially human genetics. Despite advances made in this area in the 1930s and 1940s, efforts to establish human genetics programs at universities failed to attract much interest before World War II.61 After the war, however, scientific interest in human genetics increased greatly. The American Society of Human Genetics was formed in 1948,62 and in 1954 the American Journal of Human Genetics published its first issue.63 By 1959 the society had approximately 500 members: “In the fifties, human genetics in the United States attracted a number of new recruits, both PhDs and, increasingly, MDs, aided and abetted by the opportunities for study and research available because of the government’s interest.”64 Also important for the field were many advances in medical genetics. For example, in 1948 Neel showed sickle cell anemia to be linked to a recessive gene. Chromosomal studies also furthered the field significantly. In 1959 researchers found that trisomy 21 (also known as Down syndrome) is caused by the production of three copies of chromosome twenty-one instead of the typical two copies. Physicians and medical researchers were also increasingly drawn to human genetics because of postwar advances in biochemical and molecular genetics, especially research involving enzyme deficiencies (as with inborn errors of metabolism) and studies of microorganisms and drug resistance.65 After the war, genetics was gradually added to medical school curricula and, in many cases, independent departments of medical genetics were created.66 The change was dramatic: although a “little over half the medical schools in this country and Canada in 1953 offered some instruction in genetics and only seven offered full courses in medical genetics,” by 1972 courses in genetics were required in half of all American medical schools and offered in all but a quarter.67 Federal funding for human genetics research also spiked in the 1950s because atomic age interest in the mutagenic effects of radiation became a national security concern. Thus, one funding stream for genetics was the Atomic Bomb Casualty Commission, headed by Neel,68 whose goal was to study the molecular effects of nuclear fallout. Researchers studied

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What the geneticists on the committee of the National Academy predict is a slow, almost imperceptible deterioration of the human race, a deterioration that may take centuries. It is a deterioration marked by a higher death rate, a lower birth rate, a lowered resistance to disease, a proneness to leukemia. Unless this deterioration is halted or controlled the end is just as certain as if atomic bombs were to destroy every community on earth.77

Articles like these no doubt contributed to making heredity a significant part of public consciousness. Nevertheless, apocalyptic claims about “race suicide” were refuted by many scientists and by results of the Atomic Bomb Casualty Commission demonstrating that the “only” serious effect of the US bombing of Japan was a significant increase in leukemia cases. In other words, no “frightening stories of strange after-effects of the atomic bombing” had been documented.78 And Muller, the geneticistcum-public intellectual and born again conservative, argued that fears over a race of monsters were generated primarily by communists as a way to stir up public opposition to US nuclear testing.79 Although the longterm effects of radioactive fallout were significant, Muller argued, to halt all tests and atomic research more generally would amount to a Cold War victory for the Soviet Union. In the event, the National Academy of Sciences report did not recommend an immediate halt to nuclear weapons tests. It did not even recommend a halt to the use of X-rays in medicine, the area of use the report’s authors concluded was the greatest cause for concern. Rather, the report recommended that exposure be monitored, measured, limited if possible, and, most important, studied. Thus genetics, and especially that part of the field concerned with human DNA, had been given a mandate of unprecedented importance. This mandate did not include questioning the importance of nuclear science and the atomic age it had helped to create, but it did make genetics research as important as physics, a science that had considerable cultural capital largely because of its ability to define universal laws of the material world. Genetics promised to unlock the secret laws of the life world—a point that might have become particularly important because more and more physicists were crossing disciplinary lines to study biological systems, especially after World War II.80 These disciplinary crossings also marked another important moment in the history of science and its relation to society: the retreat to the science of life would afford a safe haven from politics and ideology for physicists who

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DNA transfers information to RNA, which is then used to make proteins.89 Further elaborating the point in 1970, Crick specified that there are some “special transfers” of genetic information (for example, the transfer of genetic material from RNA to DNA in retroviruses), but there are “3 transfers which the central dogma postulates never occur”: protein to protein; protein to DNA; and protein to RNA.90 Moreover, he argued, “the discovery of just one type of present day cell which could carry out any of the 3 unknown transfers would shake the whole intellectual basis of molecular biology, and it is for this reason that the central dogma is as important today as when it was first proposed.”91 The central dogma imputed tremendous significance to the molecule that Watson and Crick had described with so much interest and passion. In part, this reflects, again, the desire of scientists like them to place biology on par with physics—to rationalize the field by proposing a simple, and more importantly, a (nearly) universal law governing the transmission of genetic information. Moreover, the central dogma was a direct refutation of any theory of acquired characteristics. According to Robert Olby, “the claim that the machinery for the transmission of this chemical specificity from DNA to proteins only allows it to operate in the one direction constituted the molecular basis for the rejection of the possibility of any form of Lamarckian heredity.”92 The central dogma was largely interpreted to mean that there is only so much genetic potential that the individual can realize, regardless of environmental context. Richard Levins and Richard Lewontin argue that the central dogma was in many ways an ideological throwback to the Weismann-inspired belief of the immortality of the germ plasm.93 But this throwback was also a means of distinguishing American genetics from Soviet genetics94—put another way, it distinguished the central dogma from the revolutionary tenet of Lamarckism that “theories which deny the reality of change are generally associated with loyalty to the status quo.”95 To understand how the DNA revolution represented loyalty to the status quo, it is important to consider the economic, social, and political context of the 1950s.96 Indeed, this decade was a time of significant transition. On the one hand, the economic prosperity of the time made it possible to continue supporting, and in some cases expand (for example, Social Security) the social welfare programs of the 1930s and 1940s. On the other hand, poverty remained a significant problem, especially for women, people of color, the elderly, and those lacking a formal education. Social reforms fell far behind social change, as when women’s wartime

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welfare programs and the role of the state in ensuring the economic security of US inhabitants. Says the historian William Chafe: “In the end, the 1950s represent more a time of transition than of stolidity. During the immediate aftermath of World War II, the possibilities for massive social change in the condition of workers, blacks, and women had been snuffed out. Instead, the appeal of the consumer culture, suburbanization, and a respite from political conflict became dominant, deflecting attention toward achievement of the material goods necessary for the ‘good life.’”99 This particular narrative of the 1950s helps us understand just what science studies scholars mean by the triumph of nature over nurture that the DNA revolution brought about. Keller, for example, writes: Of signal importance in the transfiguration of genetic determinism is the fact that, in the late 1960s, molecular biologists began to develop techniques by which they themselves could manipulate the “Master Molecule.” They learned how to sequence it, how to synthesize it, and how to alter it. Out of molecular biology emerged a technological know-how that decisively altered our historical sense of the immutability of “nature.” Where the traditional view had been that “nature” spelled destiny and “nurture” freedom, now the roles appeared to be reversed. The technological innovations of molecular biology invited a vastly extended discursive prowess, encouraging the notion that we could more readily control the former than the latter—not simply as a long-term goal but as an immediate prospect. This notion, though far in excess of the actual capabilities of molecular biology of that time, transformed the very terms of the nature-nurture debate; eventually, it would transform the terms of molecular biology as well.100

“In short,” Keller concludes, “in the vision inspired by the successes of molecular biology, ‘nature’ became newly malleable, perhaps infinitely so; certainly it was vastly more malleable than anyone had ever imagined ‘nurture’ to be.”101 The 1950s would lay the groundwork for the near permanent triumph of nature over nurture. Indeed, by the time molecular biology had obtained both the public attention and material resources it needed to be a scientific program in its own right, it was clear that the nation’s creativity, its sources of innovation, and, in short, its economic power, would be harnessed to explore the basis of life—of nature—and how to control it. Nurture would increasingly become attached to our Cold War enemy and

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devoted to embarking on a genomics project unprecedented in scale and scope; Cold War laboratory interests seeking a new mandate for the nation’s defense infrastructure; and a biotech industry that saw early on that gene sequences and the biological material used to study them were a potential source of capital it could accumulate and exchange as a result of large-scale, very fast sequencing. Moreover, several influential biomedical scientists were interested in improving mapping and sequencing technology since interest in the role of genes in disease, such as cancer, was growing considerably. Technology existed at the time to map and sequence individual genes of interest,108 but the process was labor- and time-intensive. A large sequence database, it was argued, would result in faster, more efficient ways of finding and studying genes of interest and would allow scientists to explore what, if any, importance other areas of the genome possibly held. One of the first meetings about the project was convened in 1985 at the University of California, Santa Cruz, by then-chancellor Robert Sinsheimer, a long-time molecular biology enthusiast who was interested in a project that would bring prestige to the relatively young campus.109 It was also in 1985 that Charles DeLisi (trained in physics and formerly chief of mathematical biology at the NIH), then head of the DOE’s Office of Health and Environmental Research, proposed human genome sequencing as a post–Cold War project for the DOE’s extensive infrastructure of high-tech laboratories capable of both rapid (“high-throughput”) sequencing and high-volume data storage. The DOE, long interested in genetics research (in particular, the relationship between radiation and mutation), had established the “Genbank” database in 1983 at Los Alamos National Laboratory, which could hold large quantities of sequence information.110 In 1986 DeLisi held his own workshop, similar to the one in Santa Cruz, to discuss the technical aspects of a genome project.111 Also in 1986 advocates of a large-scale sequencing project held a meeting at Cold Spring Harbor to discuss its merits.112 As in the 1950s, genetics, this time in the form of the HGP, was described in fantastical terms, likened to previous projects that had advanced scientific understanding and technological prowess in ways unforeseen when they began. Advocates also drew on the legacy of Cold War discourse, imputing to the HGP profound ontological and existential attributes, thus elevating science beyond the political and ideological fray. In a 1986 editorial in Science, Renato Dulbecco, a Nobel laureate in medicine, not only argued that a full sequence was a prerequisite for further progress in cancer

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mapping, thereby accelerating the search for specific disease-related genes (as opposed to sequencing all of the genome data first, without any regard to whether or not particular regions were important for biomedical research). This was “a type of research that many biologists wanted to pursue anyway.”125 After the release of the NRC report, James B. Wyngaarden, director of the NIH, called a meeting chaired by David Baltimore, an early skeptic (the meeting also included other critics, like David Botstein): “There, Baltimore, Botstein, Watson, and the rest of the advisory group closed ranks behind a project that would proceed along the lines recommended by the NRC committee’s report.”126 In October of 1988, James Watson agreed to head the project.127 The fact that prestigious scientists, many of whom had been highly critical of the HGP early on, came to endorse it helped shore up its scientific credibility considerably. Still, a project that would make the genome so central to biomedical science and, by extension, medical practice, would raise a number of ethical and policy concerns. Questions over employment and health discrimination, informed consent, and the potential psychological harms of genetic testing fueled much of this debate. These concerns were largely preempted by Watson’s announcement in December of 1988 that the NIH would set aside 3 percent of its HGP funds for the study of the project’s ethical, legal, and social implications—what would become known as the ELSI program. Although unexpected, Watson’s announcement was not entirely surprising since he had witnessed firsthand what can happen if geneticists appear reckless and unregulated. For in the early 1970s, scientists had successfully transplanted, for the first time, genetic material from one organism to another using restriction enzymes.128 Since recombinant DNA research involved experimentation with potentially dangerous viruses, there were obvious safety concerns, and some scientists publicly voiced them.129 The publicity resulted in research moratoriums and, more worrisome for the research community, proposals to ban the research outright.130 Watson’s decision was no doubt a shrewd one; ELSI funding would “give all the main would-be alarmists—the most likely candidates for the money, after all—a substantial interest in keeping the source of the money (the genome project) alive.”131 Thus, the history of the HGP reflects the culmination of many converging institutional interests, interests that prevailed because their opponents’ arguments were limited to the technical sphere; because social discourse was virtually nonexistent, thanks to the privileged status of reasoning in the technical sphere; and because the ELSI program had been unilaterally

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benefits, resulting in a large reduction in the number of persons receiving welfare—and for those still eligible, benefits were cut considerably.135 The Reagan administration also reversed many of the significant environmental gains of the 1970s (a topic I explore in chapter 5). These cutbacks would result, among other things, in increased homelessness, especially among the mentally ill—the very people that Koshland and others claimed would be best served by a large-scale genome project. Indeed, the Reagan years are perhaps as well known among progressives for the massive increase in homelessness among the mentally ill as they are for the “Great Communicator’s” ability to portray a social and economic landscape that would supposedly bring increased prosperity to all. Reagan, relying principally on Office of Management and Budget Director David Stockman and the latter’s embrace of the neoliberal economist Arthur Laffer, maintained that “the American spirit of individualism, competition, and personal pride would be restored, and with the shackles of government bureaucracy removed individual citizens would once again be liberated to maximize their abilities and aspirations.”136 The Reagan years would be especially hard on people of color, especially African Americans. The climate of the time was characterized by vicious attacks on blacks and by a concomitant rise in biological theories of racial pathology. Racist biologism was not limited to the likes of Richard Hernnstein and Charles Murray and their infamous (and thoroughly discredited) Bell Curve, published in 1994. By the late 1980s, the notion that violence associated with African Americans was a biological (that is, racial) trait was firmly in place, leading in 1992 to the NIH-funded Violence Initiative.137 It is within this context of significant cutbacks in the social safety net, deepening poverty, a widening rich-poor gap, and a rise in vicious and racially motivated public and scientific discourse that the largest attempt ever to make heredity foundational to the human and biological sciences was made. As in previous moments in genetics’ history, biology—especially that focused on inherited defect138—served as a salvation science, offering a rational, apolitical, and objective approach to social problems. In fact, within this salvation narrative, social problems ceased to be social at all; they were problems of human (and sometimes racial) evolution. The material devastation of the neoliberalism of the 1980s—homelessness, poverty, and environmental pollution—could now be subsumed within the discourses and practices of science. Moreover, that part of the professional and managerial class made up of salvation scientists would expand

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the existential significance of the genome project and of its ability to cure all disease, broadly defined. As I explained in chapter 1, disease is both the embodiment of social relations and the means which the analysis and critique of those relations is permanently deferred. Through the trope of health, genomics, as an institution, “explains the world in such a way as to make that world appear legitimate.”142 To examine just how this new health discourse legitimates the status quo, I turn to the BRCA (short for “breast cancer”) genes, since they became an intense object of study at the same time that the HGP was wielding its influence in the world of genetics and in public discourse more broadly. BRCA research and related projects help us understand the connection between genetic disease and the needs of both capital and the state, mediated through practices that call into being the medical subject—one that both inhabits a normatively coded body and consumes what Sunder Rajan calls the excess surplus value of the genetic test. The biological substance of biocapital, however, is both gendered and racialized; indeed, biocapital moves through bodies as well as databases and laboratory media. Indeed, the concepts of disease and health are no less ideological than those of culture and perfection.

BRCA and Genetic Disease in the Post-HGP Era In the year the HGP officially came to a close, Evelyn Fox Keller wrote that genes “have carried us to the edge of a new era in biology, one that holds out the promise of even more astonishing advances. But these very advances will necessitate the introduction of other concepts, other terms, and other ways of thinking about biological organization, thereby inevitably loosening the grip that genes have had on the imagination of the life scientists these many decades.” For Keller, the concepts “distributed program” and “developmental stability” are perhaps suitable alternatives to DNA-centered notions of “program” and “genetic stability”: We have long known that the rate of protein synthesis requires cellular regulation, but now we have learned that even the question of what kind of proteins are to be synthesized is, in part, answered by the kind of state of the cell in which DNA finds itself. In higher organisms DNA sequence does not automatically translate into a sequence of amino acids, nor does it, by itself, suffice for telling us just which proteins will be produced in any given cell or at any stage of development. Like

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of both copies of one of these genes provide the conditions for cancerous tumors to develop. Those women who inherit one bad copy of either gene at birth (the first hit) are at greater risk for this outcome—if their one good copy mutates and becomes nonfunctional due to endogenous or exogenous carcinogens or the vagaries of cellular replication (the second hit), cancer develops.151 In the 1980s, Mary-Claire King, a geneticist at the University of Washington, began investigating the link between DNA and breast cancer by studying family pedigrees and performing linkage analysis—a technique greatly enabled by new technologies developed throughout that decade.152 Then in 1990 Mark Hall, King, and their colleagues published their hypothesis in Science that a “breast cancer gene” called BRCA1, on the short arm of chromosome 17, was linked to breast cancer.153 Although only 5–10 percent of breast cancers were estimated to be of the heritable kind, King and her group hypothesized that finding the BRCA gene could help explain all breast cancer, thus broadening the impact of this research at a time when breast cancer was becoming a significant public issue.154 After the 1990 study was published, other labs in the United States and abroad, including those involved in the HGP, began the process of determining the exact location and chemical makeup of the so-called breast cancer gene. In 1994 the sequence of BRCA1 was published, and it has been confirmed that its transmission follows an autosomal dominant trait pattern.155 In 1995 another breast cancer susceptibility gene, BRCA2, was sequenced. And, in 1991, soon after the first report linking BRCA and breast cancer, Steven Narod and colleagues published the finding that ovarian cancer risk was also linked to mutations of BRCA1; it is now known that mutations of BRCA2 are also implicated in ovarian cancer incidence.156 Mutations of the BRCA genes are considered high penetrance:157 women who inherit a mutated copy of one of the genes carry a risk for breast or ovarian cancer far greater than women who have not. Nevertheless, the mutations are relatively rare, thought to be present in one out of every 300–500 people, although researchers have described mutations of these genes that are more common to discrete populations—for instance, persons of Ashkenazi descent (a topic explored more in chapter 4). In fact, a 2005 task force report recommended against routine testing of the general population, although newly updated guidelines from the American Congress of Obstetricians and Gynecologists recommend routine screening for a fairly broad segment of women.158

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For an institution to explain the world so as to make the world legitimate, it must possess several features. First, the institution as a whole must appear to derive from sources outside of ordinary human social struggle. It must not seem to be the creation of political, economic, or social forces, but to descend into society from a supra-human source. Second, the ideas, pronouncements, rules, and results of the institution’s activity must have a validity and a transcendent truth that goes beyond any possibility of human compromise or human error. Its explanations and pronouncements must seem true in an absolute sense and to derive somehow from an absolute source. They must be true for all time and all place. And finally, the institution must have a certain mystical and veiled quality so that its innermost operation is not completely transparent to everyone. It must have an esoteric language, which needs to be explained to the ordinary person by those who are especially knowledgeable and who can intervene between everyday life and mysterious sources of understanding and knowledge.166

One way that the science of genomics secured these attributes was through media discourses of the early 1990s. Genomics became a significant part of the public consciousness largely because of extensive mass-media coverage of the BRCA genes. Between 1990 and 1994, over 300 articles about the genes were published in US newspapers alone; this number does not include the many articles published about other genes believed to play a role in breast cancer.167 Inherited breast cancer research was a regular topic for major papers like the Boston Globe, New York Times, and Washington Post, as well as popular news magazines like Newsweek, which featured cover stories about BRCA1.168 This research was newsworthy first and foremost because the isolation and description of BRCA1 and BRCA2 represented a significant achievement for the genetics community. Moreover, it made real one of the promises of the HGP—that it would provide new weapons in the fight against cancer, one of the most talked about and feared diseases.169 BRCA was at times characterized as a “deadly” gene,170 and the very high risk associated with its mutations helped construct a discourse of fear. For at the time that BRCA research entered the public spotlight, it was known that mutations of the gene could increase a woman’s risk for breast cancer by as much as 85 percent over the course of her lifetime. Coupled with this fact was the belief that many more women harbored these mutations than previously thought. The president of the American Cancer Society

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the story behind BRCA1—the people that defied the skeptical research community to chart its location amid the vast oceans of the human genetic blueprint, or DNA, the people that devised the intricate techniques to manipulate our DNA in order to isolate the gene, and the people who led the furious international race to be the first to discover this precious morsel of DNA that is BRCA1.180

Reflecting on advances made by 1996, the geneticist Stephen Friend wrote that “with similar feelings as to when readers of George Orwell’s classic futuristic book, 1984, finally lived through the calendar year of its title, we are already passing through a time only imagined less than a decade ago when the first human breast cancer susceptibility gene was identified.”181 The imagery of BRCA research as a race among geneticists all over the world fit within the conflict frame the media tends to rely on and thereby helped circumvent the difficult task of reporting on a highly complex science.182 All the major papers, for example, appropriated this imagery of BRCA research as a contest to find the gene: USA Today proclaimed in one article that “the race to find the first gene linked with inherited breast cancer is over”183 and in another that “after a four-year hunt, scientists have identified a gene that causes inherited breast and ovarian cancer. The gene’s existence was discovered in 1990 and since then laboratories worldwide have raced to locate the Breast Cancer 1 (BRCA1) gene.”184 The Los Angeles Times employed similar imagery: “The race to locate the gene was ultimately won by a team of more than 45 scientists headed by geneticist Mark H. Skolnick of the University of Utah and Myriad.”185 The Atlanta Journal-Constitution referred to the research as a “decade-long treasure hunt and the beginning of a new era in cancer research.”186 Related to this, media discourse also fetishized the difficulty of genetic mapping, a not uncommon practice since genomics reporting began in the mid1980s.187 BRCA researchers, for example, were often called “gene hunters,”188 participating in the “frenzied sifting of 600,000 letters of genetic code on chromosome 17 where the gene was believed to be located.”189 Although locating the BRCA genes was difficult, given the sequencing and mapping technology available to geneticists at the time, the media’s nearly sole focus on the competitive nature of BRCA research and the sheer difficulty of finding a breast cancer gene enacted the rhetorical effect wherein describing the gene became an end in itself—a phenomenon with precedent in the public discourse about the HGP. The social history of this science was effectively erased. More than that, an implicit genetic

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breast cancer was characterized as the product of a faith-based movement driven by the tragedy of breast cancer, not a legitimate, albeit evolving, scientific hypothesis. As activists began to wield considerable political influence, representations in the media shifted accordingly. By 1998 the image of the Long Island activist had shifted from political newcomer to seasoned lobbyist and fundraiser. But rarely were the activists presented in a positive light. One of the most detailed stories to appear in the New York Times on the issue of breast cancer on Long Island did not deal with the science behind the Long Island studies but with the internal politics of breast cancer activism there. Its paternalistic-sounding title, “Growth Pains on Breast Cancer,” was followed by the observation that the movement “has evolved from a simple hands-on volunteer operation into sophisticated charitable enterprises that are increasingly being run like businesses.”199 The naïve activist is characterized as inevitably falling victim to the corrupting influences of money and power. Exhaustive details regarding how much money was raised—and how—and the political lobbying activities of group members were dominant themes. Shifts in alliances among members, including the launch of new organizations, were portrayed as problematic; unnamed “critics” and “many activists” were quoted saying that problems like “bitterness and resentment” were associated with the “power struggle to maintain their identity and receive credit for their accomplishments.”200 The fact that some people quit their jobs at various breast cancer organizations was assumed—without the benefit of elaboration or evidence—to be suspect and not, simply, the normal course of social movement evolution.201 My point here is not that the media misrepresented breast cancer activists, only that implicit in this coverage is the view that the environmental breast cancer hypothesis was inherently unscientific. In contrast, genomics was depicted as scientifically credible—which is to say, valueand interest-free. And lastly, also influencing the widespread acceptance of genomic medicine in the 1990s, was the unprecedented growth of federally funded bioethics. Paradoxically, BRCA testing became part of routine medical care amid considerable public debate about its ethical, legal, and social implications. To make sense of this apparent incongruity, one must examine more closely the fundamental assumptions of bioethics as well as the conditions of its emergence in public discourse about BRCA.202 Attention to the ethical, legal, and social implications of genetics results from two powerful stakeholder interests in genomics: industry and

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In short, the dominant narrative about the ethics of BRCA testing presumes that predictive diagnostics are powerful tools that provide lifesaving information for many women (even if the treatment options aren’t perfect), but that along with the hope and benefits of scientific revolutions come costs like insurance and employment discrimination and psychosocial distress. The best way to ameliorate these costs, according to this narrative, is to educate physicians, institutionalize genetic counseling, and protect the privacy of women. With protections like these in place, more women can reap the benefits of the genomics revolution—and in some cases help it along. For example, in an essay in the Baltimore Sun (a piece picked up by several other major papers), the legal theorist Karen Rothenberg argued that when women choose to not get tested (attributed by her to fears of employment or insurance discrimination), scientific research is the principal casualty. Regarding a specific instance, she wrote: “Understandably concerned about discrimination against herself and her children, [the woman] refused to participate in the long-term follow-up studies that could help medical science learn more about prevention, early diagnosis and treatment of familial breast and ovarian cancers. Nor will her gun-shy family participate in any more research studies, even though the benefits to future generations could be enormous.”205 Indeed, Rothenberg describes genomic medicine in such a way as to make it unthinkable that any reasonable person would refuse, provided the requisite legal protections are in place to protect insurance converge, employment, and privacy. In the same piece in which she discusses the specific case of a woman refusing to be a research subject, Rothenberg begins with a reminder that “genetic testing is indeed a scientific miracle. Never before in history have we had the amazing ability we have today, to test for genetic predisposition to common killers such as breast or ovarian cancer and heart disease. And new genetic tests for other dread diseases are appearing almost every day.”206 Public discourse about the BRCA genes—the collective result of sensationalizing genomic medicine, silencing environmentalists, and the unprecedented growth of a particular bioethics perspective—meant that the only real question addressed was how best to integrate genomics into routine medical practice.207 Yet, as the next chapter shows, what risk means, as well as who occupies the epistemological and ontological category of those at risk, has undergone a significant shift. BRCA medicine has developed in such a way that women with mutations are patients in much the same way as women with cancer. What sort of body practices have emerged as a result?

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3 Genomics and the Reproductive Body

In 2008 National Public Radio interviewed Jessica Queller, author of the book Pretty Is What Changes. In the book and the interview, Queller describes the experience of testing positive for a BRCA mutation, one that conferred upon her an 87 percent chance of being diagnosed with breast cancer and a 44 percent chance of an ovarian cancer diagnosis. These percentages presented themselves as a form of terrifying, imposing yet ultimately empowering knowledge. For Queller this meant deciding between one of two courses of action: heightened vigilance in the form of routine screening or prophylactice surgery to remove her breasts and ovaries so that she could, as she put it, defy her destiny. And, as the title of Queller’s book suggests, contemplating surgery of this kind is tantamount to radically questioning hegemonic notions of femininity and beauty. At the time of the National Public Radio interview, Queller, then thirtyfive, had already undergone a double mastectomy; she had decided to postpone having her ovaries removed. The reason for this deferral? She desired marriage and children, so the decision to undergo an oophorectomy would have to wait—even though her mother had died of ovarian, not breast, cancer. We see, then, in Queller’s narrative how gender norms are reestablished in the process of becoming a patient. As Queller said in a later interview, referring to her breast reconstruction surgery, “you’re really put back together again beautifully.”1 Queller’s story, as it turns out, represents the most recent twist in an evolving discourse of gendered medicine. For women at BRCA-related risk for breast cancer, oophorectomy, the prophylactic removal of ovaries, helps them reduce that risk while avoiding the visible scars of mastectomy. Yet at the same time, plastic surgery techniques have advanced >>

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Ovarian Cancer and Heredity Ovarian cancer stands out among the reproductive cancers affecting women. According to the American Cancer Society, in 2004 approximately 26,000 women were diagnosed with ovarian cancer, and 16,000 did not survive.4 The National Cancer Institute predicts that in 2011, 22,000 women will have been diagnosed and 15,500 will have died.5 Estimates for 2012 are basically the same.6 Indeed, ovarian cancer causes more deaths than any other cancer of the female reproductive system.7 As is the case with many other diseases, the statistics also reveal disparities. Black women, for instance, are less likely to get ovarian cancer than white women, but they are more likely to die from the disease (a pattern similar to that of breast cancer). Moreover, trends suggest that while incidence and mortality is declining overall for white women, for black women both have remained steady.8 The consensus in the literature is that early detection will not reduce mortality rates to an appreciable degree. Although technologies such as transvaginal sonography and the cancer antigen blood test known as the CA-125 screen are available, the evidence is mixed as to whether they can reliably and consistently detect the disease at an early stage and improve survival (ovarian cancer is very deadly once it progresses beyond stage I—when it is still quite localized). As a result, these detection procedures are not routinely performed, unlike mammography for the early detection of breast cancer and pap smears for the early detection of cervical cancer. Most ovarian cancers, then, are diagnosed at stage II or later, the result being an extremely high death rate. Identifying women at higher-thanaverage risk so that they can undergo detection procedures has, understandably, been a goal of cancer researchers and at-risk women. Well before the first BRCA gene was mapped, interest in a genetic predisposition for ovarian cancer was sparked by knowledge of the so-called hereditary cancer syndromes. These syndromes explained why in some families, many women—especially young women—were diagnosed with breast and/or ovarian cancer. A study based on the Gilda Radner Familial Ovarian Cancer Registry from 1981 to 1991 established that ovarian cancer risk could indeed be understood as a genetic predisposition for some families.9 In those cases where two or more first- and second-degree relatives were diagnosed with ovarian cancer, risk was apparently linked to an autosomal dominant trait. The researchers studying families in the Radner Registry found that the vast majority of such cases were motherdaughter and sister-sister pairs.10 The risk for women with a family history

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Not all recommendations for prophylactic oophorectomy have been so strongly worded, largely because scientific evidence demonstrating the efficacy of oophorectomy was limited prior to 2002. Particularly problematic was the fact that no prospective studies comparing women electing surgery with women electing surveillance had been carried out, and in the retrospective studies that did show a benefit from the surgery, the subjects did not have BRCA mutations. A Consensus Statement by the Cancer Genetics Studies Consortium organized by the US National Human Genome Research Institute did not include an explicit recommendation for oophorectomy, writing that “observational data have so far failed to demonstrate statistically significant evidence for risk reduction.”20 Much of the concern over oophorectomy was the result of researchers’ observations that up to 10 percent of women undergoing oophorectomy were diagnosed with ovarian-type cancers years later.21 These women were diagnosed with peritoneal carcinoma, a disease indistinguishable from ovarian cancer.22 Qualified language concerning prophylactic oophorectomy was quickly replaced with enthusiastic assessments after the publication of two studies demonstrating that ovarian cancer risk can be lowered after oophorectomy for BRCA carriers. In one study, by Noah Kauff and coauthors, after a mean follow-up of two years, one out of ninety-eight women who had oophorectomy developed cancer (peritoneal), compared to five out of seventy-two women who elected to undergo surveillance only (four had ovarian cancers, one peritoneal cancer). In the other study, by Timothy Rebbeck and coauthors, 2 out of 259 women undergoing oophorectomy were diagnosed with peritoneal cancer during the approximately eight years of follow-up, compared to 58 out of 292 women who opted for surveillance only and were later diagnosed with ovarian cancer. For the Kauff group, the results provided “strong support for including discussion of risk-reducing salpingo-oophorectomy as part of a preventive-oncology strategy for women with a BRCA1 or BRCA2 mutation.”23 Rebbeck and coauthors wrote: “On the basis of the results of our study, we advocate prophylactic oophorectomy to reduce the risk of ovarian and breast cancer in women with BRCA1 or BRCA2 mutations.”24 These 2002 oophorectomy studies are widely cited in the cancer genetics literature as scientific evidence that the procedure is, on the whole, beneficial for women with BRCA mutations. Writing in the Journal of Clinical Oncology in 2003, Douglas Levine and colleagues claimed that “risk-reducing salpingo-oophorectomy is currently recommended for

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Kingdom. It has also played an important part in the emergence of medicine as a key site for the surveillance and disciplinary control of women’s bodies. To properly situate contemporary oophorectomy historically requires an examination of the many justifications for ovary removal over time—justifications that reflect social values concerning gender, reproduction, and motherhood. Ornella Moscucci has noted that gynecology is a “specialism which is underpinned by a historically contingent notion of woman.”29 In turn, gender roles have obtained social legitimacy by way of elite medical discourse.30 Specifically, the ovary was, in the nineteenth century, key to the reigning model of femininity.31 The first successful ovariectomy, attributed by many historians to Ephraim McDowell, a physician practicing in Danville, Kentucky, has also been described as the “first successful elective exploratory laparotomy in the world.”32 In 1809 the unidentified female patient endured what was acknowledged by McDowell to be an experimental surgery without the benefit of anesthesia or antisepsis (the former was not available, the latter not considered important) to remove a large ovarian cyst. Subsequently, throughout the early 1800s, surgeons pursued their interest in ovariectomy, largely in the effort to advance their craft and establish gynecology as a legitimate field of medicine and to treat ovarian disease that they argued was grave enough to warrant life-threatening surgery. “During [oophorectomy’s] heyday doctors boasted that they had removed from 1,500 to 2,100 ovaries apiece.”33 Critics, however, were quite forceful in their attacks, calling these surgeons “belly-rippers,” responsible for the death of women with medical conditions that were not necessarily fatal.34 “By the mid-1800s,” writes Moscucci, “ovariotomy was in dispute.”35 Nevertheless, the procedure continued to be performed, as it was both lucrative and central to the professionalization of gynecology—at the time a young specialty. Specifically, ovariotomy helped gynecology emerge as a reputable and indispensable area of medicine that could compete with the already established field of obstetrics.36 Mortality rates from ovariotomy gradually declined, in part due to the development of effective antisepsis. Yet the most significant development was the introduction of anesthesia,37 a development that undermined critics’ arguments that the surgery was, in effect, a form of inhumane experimentation on women. Practitioners at this time also drew connections between women’s reproductive organs and their “nature” in order to secure for gynecology a role in the rather lofty debate about gender and society. Referring to the

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were apparently so successful that it was soon performed for ‘all cases of lunacy’ and young surgeons would be given an annex of a psychiatric hospital where they would remove ovaries from the inmates.”48 The emergence of the so-called normal ovariotomy is but one manifestation of the general belief that reproductive organs were central not only to a woman’s identity, but also to her physical and mental health, broadly defined. Importantly, the health of white, middle-class women was viewed as crucial to the security and stability of the nation. Indeed, early eugenicist thinking pervaded gynecological discourse, especially with regard to the connection between ovarian disease and mental illness: “From one perspective, the castration of women starting in the 1870s (performed overwhelmingly on noninstitutionalized outpatients, and only later—in the 1890s—on inmates of mental institutions) was part of the general anxiety about the racial future of white America.”49 Articulating the social importance of gynecology, Lawson Tait, one of “normal” ovariotomy’s namesakes, observed: “To the naked eye nothing could look more uninteresting and unimportant than the human ovary; and yet upon it the whole affairs of the world depend.”50 What exactly threatened the ovary and, in turn, the social order in the United States in particular? For public intellectuals, cultural critics, and physicians alike, white, middle-class women’s push for education, entrance into the public sphere (to initiate and participate in reform campaigns, most notably for temperance and the franchise and against slavery), and fight for reproductive autonomy called into question popularly held beliefs about gender.51 Contested ideas about women, motherhood, and femininity further threatened national identity—indeed, the nation itself. An educated woman, they argued, was less likely to reproduce, and women who were involved in the political realm were likely to neglect their expected duties in the private sphere, thereby jeopardizing the next generation of citizens and leaders. Especially during the latter part of the nineteenth century, worries over the American woman’s physical fitness stirred fears of race suicide: “The young women of the urban middle and upper classes seemed in particular less vigorous, more nervous than either their own grandmothers or European contemporaries.”52 The putative “deterioration” of women “called gynecology into existence,” according to the physician Augustus Kinsley Gardner.53 Scientific discourse further served a critical disciplinary function: “Since at least the time of Hippocrates and Aristotle, the roles assigned women have attracted an elaborate body of medical and biological justification.

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about women, motherhood, and nation to reduce the number of surgeries performed. Male physicians and women activists benefited strategically from the symbolic importance of ovaries, arguing that ovariotomy stripped women of their identity (the charge of “desexing” women was common), an identity largely rooted in motherhood and its connection with nationalism and the imperialistic imaginary:60 “Flagrant abuse of the procedure, its hazards and questionable results, but above all the gradual realization that ovaries are precious organs [William Goodell presiding (over) the 3rd annual meeting of the American Gynecological Society in 1875 thought fit to remind his audience that ‘woman is so called because she bears a womb’ and ‘physiologically she is a woman because she owns two ovaries’] caused the pendulum to swing and initiated the downfall of Battey’s operation.”61 The historical narrative I have thus far constructed shows how oophorectomy has served the institutional interests of surgeons (specifically gynecologists) since the early part of the nineteenth century. The procedure also figured centrally in debates about women, their reproductive organs, and the social order at large. When ovariectomy for explicitly cultural reasons fell out of favor, ovarian cancer would present gynecologists with the opportunity to fight a deadly disease requiring nothing less than radical intervention. A positivist perspective, informed by a logic of progression, would hold that this transition to cancer prevention is simply the expected outcome as gynecology passed over into a more enlightened period of its history. A social, materialist history of gynecological surgery asks instead what this new reconfiguration of objects, patients, practices, and social relations actually means in terms of particular interests served.

Oophorectomy’s New Legitimacy Crisis By the turn of the century in both the United States and many European nations, “only diseased ovaries tended to be removed.”62 The meaning of “diseased” was open to interpretation, however, and ovariectomy was still performed in order to remove benign growths. Moreover, what some historians have described as the “discovery” of ovarian cancer as a public health threat lent support for the prophylactic removal of ovaries even by those who had previously supported ovarian conservation. The insidiousness of ovarian cancer (frequently characterized as a form of so-called creeping death), more than its actual incidence, accounted for the revival of oophorectomy. As one gynecologist wrote in 1942, “the involuting63

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women at average risk for ovarian cancer is more controversial and is discussed below). For example, the authors of a 1997 review wrote that “prophylactic oophorectomy during benign pelvic/abdominal surgery is recommended for women who have a significant family history of ovarian cancer and have completed child bearing or for women aged >40 years.”75 Such a recommendation accommodates the desire of some women to have children; it further rests on the assumption that postmenopausal ovaries are no longer an important component of a woman’s endocrine system. In short, after menopause, ovaries are superfluous and can do only harm: “If the woman is already menopausal [and undergoing pelvic surgery for another condition], it [is] well worth counseling her of the entity of ovarian cancer, as many are not aware of the condition. There is no good reason to retain menopausal ovaries, as the risk of developing ovarian cancer increases with age” (emphasis added).76 Although no physician would recommend that a woman at average risk for ovarian cancer undergo surgery for the sole purpose of removing her ovaries,77 the practice of removing them if the surgical occasion presents itself is widely accepted. This belief is underscored by concern that, often, the condition or conditions necessitating surgery in the first place are part of a generalized disorder, sometimes called “residual ovarian syndrome,”78 that will probably require additional major surgeries in the future, thereby exposing women to unnecessary risks (including those posed by anesthesia), significant recovery time, and, perhaps, decreased quality of life.79 “Since the 1950s,” observed two cancer researchers, “the issue of prophylactic oophorectomy has been plaguing the surgeon. Studies have confirmed that 4.5–14.1 percent of women develop ovarian cancer after hysterectomy for non-ovarian conditions. Similarly, data from the American College of Surgeons demonstrated that among 12,316 patients with ovarian cancer, 18.2 percent had previous hysterectomies with conservation of one or both ovaries and 57.4 percent of these women were over the age of 40.”80 In 2005, however, the rationale for routine oophorectomy at the time of abdominal surgery was called into question by the publication of a decision model (a method of cost-benefit analysis) showing that prophylactic oophorectomy heightens risks of death from heart disease and osteoporosis, risks significant enough that they probably outweigh the benefit of lowered risk for ovarian cancer.81 The researchers—who were from the University of California, Los Angeles; the University of Southern California; and the University of Auckland—claimed that the study

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model’s operating assumptions (for example, that few women would have HRT) and concluded that “the decision analysis reviewed here is not informative, and it offers no guidance to gynecologists in deciding whether or not to remove the ovaries when performing hysterectomy.”87 Davy and Oehler claimed it was premature to dismiss post-oophorectomy interventions that could help reduce long-term mortality, such as HRT, statin therapy (for reducing cholesterol), and bone density correctives, warning that in comparison “there is no prevention for ovarian cancer but oophorectomy.”88 They continued: “It is unlikely that many surgeons are going to change their management based on the current controversy.”89 John Studd, the physician openly critical of late-nineteenth-century routine ovariectomy, took a somewhat different approach and, in addition to championing modern medicine’s ability to prevent or reduce the morbid effects of prophylactic oophorecotmy, characterized advocates of the procedure as courageously sticking to principle in the face of “fashionable” and “politically correct” criticism (he claimed in 1989 that oophorectomy should be performed for all women over the age of forty when having abdominal hysterectomy).90 Studd’s most pointed attack was directed at the assumption that women do not comply with recommended HRT schedules. It is the responsibility of the surgeon, he argued, to deal aggressively and vigilantly with women who resist the therapy. In response to the preponderance of evidence that side effects of HRT accounted for women’s reasonable resistance to it, Studd wrote: “Even if there are side-effects to replacement therapy, it would be hard to believe that estrogens are more dangerous than conserved ovaries with their malignant potential as well as their endogenous production.”91 He concluded by calling for randomized trials as a way to definitively determine the benefits of prophylactic oophorectomy for women at average risk, even though he surely knew no study of the kind would ever pass ethical muster.92 Still, Parker and his colleagues did have their supporters, suggesting that the model would, at the very least, motivate the medical community to reexamine the practice of routine oophorectomy. One physician wrote: “The decisions by patients and their doctors can now be based upon better facts rather than just ‘what is done.’”93 David Olive echoed this sentiment in an editorial in Obstetrics and Gynecology, adding that clinical practice would probably be altered (a change that might be “time-consuming and annoying to some”), an important shift because “even if no coronary heart disease increase is seen with oophorectomy, there remains no demonstrable advantage to the procedure in terms of longevity!”94

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Esther Eisenberg of the North American Menopause Society, “for most women, the scales are now tipping towards ovarian conservation.”106 Emily Martin has written that it is easier to see the connections between science and society from the privileged vantage point of the historian.107 Nevertheless, these connections remain in the contemporary moment. To be sure, the most recent oophorectomy controversy forces us to question positivist histories of science and medicine and the logic of progress on which they depend. The routinization of oophorectomy for cancer prevention is no less a sociopolitical phenomenon than was routine oophorectomy in the nineteenth century. What the entire history of oophorectomy tells us is that changes in clinical practice are inextricably linked to societal attitudes about the body at risk as well as to the conceptual and professional needs of researchers and physicians. In the early part of the nineteenth century, the availability of women’s bodies (largely the result of prevailing ideas about reproductive organs, motherhood, and gendered frameworks of disease assessment), coupled with the need to advance surgical techniques and solidify the relevance and sophistication of gynecology, made oophorectomy a popular—and abused—procedure. Today the state of scientific knowledge about ovaries plays a significant role in making their removal thinkable largely because the ovary is metonymically reduced to its reproductive role. As the authors of a research review concluded, “the normal physiology of the post-menopausal ovary has not been extensively studied, and it is possible that removal of the post-menopausal ovaries may have greater consequences than has previously been believed. It is clear that the effects of bilateral oophorectomy in pre- and post-menopausal women at the time of hysterectomy are a fertile ground for clinically significant research.”108 In other words, the scientific community is only now beginning to take seriously the role of ovaries in a general economy of health, suggesting that these organs have remained both the biological and the symbolic seat of femininity and motherhood longer than has been acknowledged. Nevertheless, oophorectomy will continue to capture the attention and interest of gynecologists and cancer specialists as it has a new constituency: the BRCA mutation carrier.

Constitutive Discourse and the Medical Subject As the revised ACOG guidelines illustrate, the gynecology community has recognized the need to rethink oophorectomy. But ACOG—as well as both the Parker and Rocca research teams—emphasizes that treatment for

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as a heritable trait. In fact, their very purpose was to address the concerns of cancer physicians that genetic testing would fuel interest in the procedure. One physician wrote: “The identification of the BRCA genes and the availability of genetic testing for BRCA mutations have underscored the need for improvements in early detection and prevention of breast and ovarian cancer.”111 And since the studies by Kauff and colleagues and Rebbeck and colleagues showed that BRCA mutation carriers in particular would benefit, calls for more genetic testing have followed.112 Geneticists distinguish BRCA tests from analyses of family history in a number of important ways. Unlike family pedigrees, they say, BRCA tests bring “the promise of reducing uncertainty surrounding [BRCA carriers’] risk status, thus enabling them to make more informed decisions about whether to undergo prophylactic surgery” (emphasis added).113 According to the authors of a review essay, recent insight into the hereditary nature of some cancers and the advent of genetic testing have made risk assessment increasingly accurate.”114 Family history, once an important factor in assessing a woman’s risk, has increasingly become regarded as inaccurate and inferior. Writing in the Journal of Clinical Oncology, researchers from cancer centers in the United States and Canada concluded that “the strongest risk factor for ovarian cancer is the presence of an inherited mutation in 1 of the 2 ovarian cancer susceptibility genes, BRCA1 or BRCA2.”115 As one author put it, family history alone is a “poor predictor.”116 Yet the risk associated with BRCA mutations, much like the concept of risk more generally, is not objective fact, but a social construct.117 Both family pedigree data and BRCA tests produce statistical probability statements—the telos of both types of analysis is to establish risk, not diagnose disease. They tell a woman, based on clinical evidence, whether she is at significant risk and, thus, whether she should consider radical therapies. Before the BRCA test, risk was based on data from registries as well as familial and environmental history. In the wake of the test’s commercialization, risk is now calculated based on the structural features (and presumed function) of the mutation that the woman has inherited. Clinical data are limited to the study of only some of the thousands of known mutations. Risk assessment, then, is the determination that the chemical makeup of the mutation does or does not suggest that it is “deleterious,”118 not necessarily whether clinical data do or do not demonstrate the approximate risk it confers. Regardless of the method used, both types of risk assessment presume risk to be variably penetrant. Before genetic testing, women with a strong family history of ovarian cancer were told their risk was as high as 50

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screening methods such as sonography and CA-125 serum testing, which can detect only actual cancer. BRCA tests have become, in the words of cancer researchers, substitutes for screening: they are a method of true prevention.126 Moreover, cancer surgeons have reported finding ovarian cancer tumors during oophorectomy, bestowing on the procedure an entirely different, unexpected purpose: early detection. As such, it has provided material evidence for the cancer surgeon that genetic risk is never merely risk. The elevation of BRCA tests as a form of primary (and thus superior) surveillance is inextricably linked to the routine dismissal of the alternatives. It is not uncommon for researchers to discount the efficacy of secondary screening despite conflicting evidence regarding the effectiveness of sonography, especially for women with a family history of ovarian cancer.127 At best, researchers characterize the extant data as mixed; at worst, they claim that “no screening for ovarian cancer has yet been proved effective for women in any risk category” (emphasis added).128 In 2006, shortly after the publication of the Parker decision model, the endorsement of oophorectomy became even more emphatic: “Ovarian cancer is, in most cases, a lethal disease as it is virtually impossible to diagnose at an early stage, and almost impossible to treat successfully when detected at an advanced stage. Thus, any means we have of reducing the incidence of the disease should be embraced” (emphasis added).129 Yet as early as 1991, some researchers were reasonably optimistic about the benefits of another kind of screening for women at high risk: TVS [transvaginal ultrasonography] is particularly effective as a screening method in women whose primary or secondary relatives have documented ovarian cancer. By limiting screenees to those with a positive family history of ovarian cancer, the authors found that the prevalence of ovarian cancer in the screened population increased 10-fold. As a result, the positive predictive value of TVS increased proportionately. Three primary ovarian cancers were detected in 776 asymptomatic women. All three women had Stage I disease and all are now alive and well.130

Conceivably, the use of TVS in the above study presumes that hereditary ovarian cancer is a variably penetrant disease necessitating the assessment of family history and a cautious, less intrusive approach to prevention. In contrast, BRCA mutations necessitate no less than surgery, betraying the belief among researchers that risk is functionally 100

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unquestioned. Although ovaries are no longer removed for so-called psychic disorders, cancer prevention has replaced this earlier rationale for prophylactic removal. Similar to abusive practices of the past (for example, Battey’s or Tait’s operation), the current model of ovarian cancer prevention rests on unquestioned and/or flawed assumptions—today, those stemming from static, woefully underdeveloped theories of ovarian function133 and the concomitant inability of medicine to model these functions effectively. Still, the recent debate about prophylactic oophorectomy for women understood to be at average risk for ovarian cancer inaugurates an important moment in this history: the studies by the Parker and Rocca teams, irrespective of methodological limitations, destabilize the foundation on which this procedure has heretofore been carried out. Despite the inertia of standardized, routinized medical procedure, there may be some chance that reflective examination of practices will continue in earnest, as well as the pursuit of much-needed research on the multifaceted function of ovaries throughout the life span. Yet, as I discussed in the previous section, even within the pages of these articles and the responses to them, there remains one clearly stated exception to the findings: the BRCA mutation carrier. As Parker and colleagues make clear, their analysis pertains to women with average risk for ovarian cancer, not women with the higher risk associated with inherited mutations of the BRCA genes. Even with the increase in mortality associated with oophorectomy, the information that a BRCA test provides is sufficient to justify the surgery. On closer examination, however, many of the criticisms of routine prophylactic oophorectomy apply to BRCA carriers as well, thus inviting critical reflection about their putatively distinct medical status. The wide range of risk for ovarian cancer (10–60 percent) among BRCA carriers at the very least necessitates the assessment of the risks associated with surgical, early menopause. There are, moreover, considerations specific to BRCA carriers who contemplate prophylactic measures. First, although oophorectomy significantly reduces the risk for ovarian cancer, it does not completely eliminate it. The studies by the Kauff and Rebbeck teams published in 2002 did show a dramatic decrease in ovarian cancer. However, for some women the procedure did not decrease risk for peritoneal cancer—a phenomenon that has been observed for some time and that proves what Andrea Eisen and Barbara Weber have called BRCA’s “field” effect.134 In a third study published in 2002, a different team of researchers concluded that “the majority of the ovarian-type

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This reasoning makes sense only for women who have an 85 percent lifetime risk for breast cancer (if it makes sense at all). It ignores the well-documented variability of BRCA-linked breast cancer risk, and it overlooks the fact that many women test positive for mutations for which no clinical trial evidence exists. The Grann model further assumes that the risk for heart disease in women with BRCA mutations is the same as in women in the general population, despite evidence suggesting that the risk may be higher for women experiencing surgical menopause. And finally, the model assumes that all women face the same risk for mortality from ovarian cancer, even though some studies show that women with BRCA mutations have a better chance of surviving that cancer than women without mutations.143 Even with the contestable assumptions of the Grann model, the greatest life expectancy gain predicted is 4.6 years for a thirty-year-old woman who undergoes oophorectomy and chemoprevention. A different model predicts more modest gains: 0.3–1.7 years for a thirty-year-old woman who chooses oophorectomy.144 Neither model takes into consideration spotty HRT use over time or evidence that early, or premenopausal, surgical oophorectomy can be dangerous. Regarding the latter point, it is certainly not the case that the health benefits of intact ovaries are completely ignored by researchers. Nevertheless, the treatment decision calculus presented in studies of the relative benefit of oophorectomy does not take intact ovaries to be important enough to weigh against the benefits of cancer prevention. The short- and long-term side effects of oophorectomy often recede, rhetorically, in a discourse in which the only goal is reducing cancer risk, seemingly at any cost. In one influential study supporting the efficacy of oophorectomy, the researchers first construct a decision calculus that clearly downplays the side effects associated with oophorectomy: The primary negative consequence of prophylactic oophorectomy in premenopausal women is premature menopause, which may be associated with increased risks of osteoporosis and cardiovascular disease. Hot flashes, vaginal dryness, sexual dysfunction, sleep disturbances, and cognitive changes associated with menopause may affect the quality of life. However, the risk is balanced by the morbidity and mortality associated with breast and ovarian cancer in carriers of BRCA1 or BRCA2 mutations, and these symptoms may be managed by hormonal or nonhormonal medications.145

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converged, creating a new constituency for the long-embattled procedure. Describing the material influence of BRCA testing on ovarian cancer prevention, Kenneth Offit, a well-known oncologist, said: “We are beginning to believe that we may be showing some first evidence of lives saved because of the genetic testing we are doing. . . We have now followed over 200 women with BRCA mutations, and we have found four early-stage ovarian cancers in almost 100 preventive surgeries. For many of us, it is exciting. I have been at Memorial for 10 years and didn’t see a stage I ovarian cancer until we started doing BRCA testing. . . These developments have energized investigators to press ahead.”149 In a mutually beneficial turn of events, oophorectomy imbues the BRCA research agenda with a measure of legitimacy it had previously lacked. Widespread acceptance of the BRCA test has been hampered by the dearth of options available to women should they learn that they carry an inherited mutation. And of those options, most are radical, like prophylactic mastectomy, oophorectomy, and pharmaceutical treatments. One study noted: “Further information on the benefits of genetic testing might help women to make decisions about whether to have genetic testing, and will allow women to use information gained from testing in an optimum way that will improve clinical outcome.”150 The legitimacy of prophylactic oophorectomy is further bolstered by its association with reduced risk for hereditary breast cancer.151 The Rebbeck and Kauff teams concluded that prophylactic oophorectomy reduced not just ovarian cancer risk, but also breast cancer risk for the women they studied. Since then, several researchers have speculated that women would in fact prefer oophorectomy to mastectomy to avoid the disfiguring consequences of the latter.152 The established efficacy of oophorectomy, moreover, has led to calls for more genetic testing as well as for including the surgery as an option in counseling women at risk for breast cancer whether or not they have inherited a BRCA mutation. One physician wrote: “The effectiveness of prophylactic oophorectomy in carriers of BRCA mutations provides a strong rationale for genetic testing in women with a strong family history of breast cancer.”153 And in 2001 researchers from the United Kingdom advised: “Epidemiological studies suggest that prophylactic oophorectomy may play a role in the prevention of breast cancer in high risk populations. Therefore, there may be a case for informing women at risk of breast cancer about this option.”154 So strong is the suspected benefit of prophylactic oophorectomy for reducing breast cancer risk that it is slowly becoming a thinkable strategy for the

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an attractive approach to treatment. Important, too, is the influence of women’s health advocacy. The disfiguring effects of radical mastectomy, especially the version popularized by William Halsted, catalyzed the modern breast cancer movement and the eventual decline of both the radical mastectomy and the surgery’s other varieties. Nevertheless, although lumpectomy has largely replaced mastectomy for women in the general population diagnosed with breast cancer,161 prophylactic mastectomy is recommended for women with BRCA mutations,162 and so alternatives to mastectomy are still a topic of concern for this group of women.163 In their evaluation of statistics regarding prophylactic mastectomy and prophylactic oophorectomy, Andrea Eisen and coauthors claim that the numbers reveal more interest in the latter, due to the “absence of externally visible physical changes.”164 The emergence of oophorectomy for the treatment and prevention of breast cancer provides, in serendipitous fashion, a new rationale for the surgery at a time when its legitimacy is being challenged in other areas of gynecological medicine. BRCA genomics in turn (and genomics more generally) requires evidence-backed interventions that will help make genetic testing more attractive to women at risk. What the literature on oophorectomy and breast cancer also reveals, however, is how gender norms both shape and are shaped by the discourse of heredity and the female body. As this chapter has already shown, the metonymical reduction of ovaries to their reproductive function has been absolutely key to the exception made for BRCA mutation carriers. When cancer researchers effectively dismiss the health importance of ovaries as well as the complexities that HRT presents for these women, they presume that ovaries enable procreation but nothing else beneficial or productive. Thus, ovaries are dispensable for women who no longer need or want them for the purpose of reproduction. In the literature on oophorectomy and breast cancer, sex is similarly gendered. Ovaries are clearly distinguished from breasts when one accounts for the preference by women and their doctors for one surgery but not another. The distinction is only possible because of the presumed difference between visible and invisible sex organs (or, one might say, the difference between sex organs and reproductive organs). Statements regarding the superiority (aesthetically speaking) of oophorectomy imply that breasts are visible markers of femininity and sexuality in ways that ovaries are not. Invisible to the naked eye, ovaries are not part of the gendered economy of signs in the way that breasts are.165

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be diagnosed with ovarian cancer at the same age as women in the general population, may conclude that risk for heart disease and osteoporosis weighs heavily against the benefits of early oophorectomy.168 The rhetoric of timing, moreover, determines whether a woman can in fact exercise motherhood as an exceptional state, and it does so by trafficking in mainstream, accepted gender norms. If, for instance, a woman contemplates postponing oophorectomy beyond the age of thirty-five, her physician will have to consult a medical literature that has already determined such a risk to be unacceptable, especially if the woman in question is a BRCA1 mutation carrier (recall that women with BRCA1 mutations tend to be diagnosed six to nine years earlier than women with BRCA2 mutations).169 This disparity in the timing of cancer diagnoses “has significant implications,” the authors of one study argue, “for counseling BRCA mutation carriers regarding the timing of preventative interventions.”170 For BRCA1 mutation carriers, early motherhood is necessary in order to reap the benefits of prophylactic surgery (although, interestingly, BRCA2 mutation carriers are never presumed to have good reason to postpone oophorectomy beyond the age of thirtyfive, or to refuse it entirely). In short, reproductive options cannot be fully retained without incurring some health risks: With regard to the question of timing, there is uniform consensus, for obvious reasons, that risk-reducing salpingo-oophorectomy should be deferred until childbearing is complete. However, as more of our patients delay child bearing into their late 30s and 40s, BRCA1 mutation carriers, in particular, begin to expose themselves to a nontrivial rate of ovarian cancer (11–21 percent by age 50). Although carriers of BRCA2 mutations are at less risk of ovarian cancer during the reproductive years, mutation carriers who defer oophorectomy until the 40s and beyond may lose the substantial protective effect of salpingo-oophorectomy against breast cancer [emphasis added].171

Presumably, cancer researchers have chosen the otherwise arbitrary age of thirty-five because, in the field of obstetrics, it is the number that separates young from so-called advanced maternal age.172 Yet fertility trends show that women are having children later in life, often well into their thirties and early forties.173 Within this context, to say that age thirty-five is the cutoff for childbearing is to say that it ought to occur relatively early in life.

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was always already gender, with the consequence that the distinction between sex and gender turns out to be no distinction at all. It would make no sense, then, to define gender as the cultural interpretation of sex, if sex itself is a gendered category. Gender ought not to be conceived merely as the cultural inscription of meaning on a pregiven sex (a juridical conception); gender must also designate the very apparatus of production whereby the sexes themselves are established. As a result, gender is not to culture as sex is to nature; gender is also the discursive/ cultural means by which “sexed nature” or “a natural sex” is produced and established as “prediscursive,” prior to culture, a politically neutral surface on which culture acts.178

Reproductive organs (“sex”) serve to gender bodies materially and socially; reproduction, says Butler, has become the only salient feature of sex, even though there are many bodies that resist or simply exist outside of this grid of intelligibility.179 In the present case, ovaries are the site of the imposition of gender norms, a disciplinary effect of culture that is masked by the power of biomedical discourse to present the biological body as natural fact. If the biological body is always already gendered, it stands to reason that reproduction would be the sole exception to oophorectomy. Ovaries are engines of procreation or creeping death, and this binary governs the body in two ways: first, by tacitly enforcing norms of motherhood (in particular, young motherhood); and second, by securing the body as an object of surveillance and intervention by the field of cancer medicine. Although it is not possible to live wholly outside of such discursive constraints, it is nevertheless the case that the enactment of gender norms is not entirely successful all of the time. Some bodies are not fully intelligible according to the logics of normative sex or gender and so could be said to challenge or resist them in some way. These bodies provide an occasion—if only a fleeting one—to comprehend the performativity of the gendered body: the supposed failure to repeat, or properly enact, gender opens up the possibility for questioning its biological (or even metaphysical) substance. The intersex are a case in point: the intersex body defies the traditional male and female sex categories, whether they are defined by chromosomes, hormones, genitalia, or reproductive organs. With the recognition among feminist social theorists and science studies scholars that sex is no more a biological fact than gender is, even though the successful enactment of gender provides the illusion that it is,

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young motherhood and the pathologizing of the same (and, indeed, of motherhood in general) for African American women within the larger culture.181 Indeed, throughout history discourses of motherhood and feminity have been structured around the presumption of racial difference. Put another way, they are racialized. Early twentieth-century diseasing of white women’s reproductive organs was possible because of the belief that the exercise of their rights compromised reproductive capacity and thus posed a threat to the social order, culminating in eugenicist fears of race suicide. In contrast, in the case of black women, the source of such threats was their presumed hypersexuality and fertility. Whatever the paradoxical relation oophorectomy had to this differential cultural imperative to reproduce, the importance of white fertility was never in doubt and, indeed, provided a narrative that critics of the surgery could appeal to during nineteenth-century debates. As Dorothy Roberts and Rickie Solinger have both documented, policymakers and public intellectuals of all political persuasions have typically directed their ire toward black women, rather than institutional racism, when trying to explain phenomena such as poverty and crime.182 What has resulted are differential practices of hysterectomy and sterilization along the axis of race.183 As discussed in chapter 2, sterilization was a popular surgery beginning in the early twentieth century, escalating in the 1920s with the rise of negative or mainline eugenics. Although the demise of the eugenics movement reduced the number of sterilizations performed, involuntary and coerced sterilization of US black women continued well into the 1970s.184 Moreover, implantable and injectible contraceptives such as Norplant and Depo-Provera effectively sterilize women because they induce long periods of infertility and, in the case of implantables, require costly medical visits to remove.185 Today, sterilization is one of the most common forms of birth control for African American women in the United States.186 And although hysterectomy rates have been artificially high for women across class and race, they are particularly high for black women. When the ovaries of black women symbolize reproductive capacity, they are targeted for removal. When they are cancerous and pose grave threats to life, they no longer serve as objects of radical intervention—a reverse of the logic I described in the previous section, when, presumably, the bodies in question are white. Regarding gynecological cancer, differences in mortality from ovarian cancer are explained in part by the fact that African American women are more likely than white women to be diagnosed at an advanced stage of the disease and in part by the

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One explanation for this discrepancy appeared in a 2003 article in the Journal of the National Cancer Institute, in which the authors suggested that when young women become pregnant, a window of vulnerability opens that may make them more susceptible to malignancies.191 In this way, the study seemed to lend credence to Nancy Krieger’s 1989 critique of the estrogen hypothesis, in which she argued that many patterns of breast cancer incidence contradict the putative impact of endogenous hormones like estrogen and that exposure to external carcinogens at particular times during the development of the breast probably explains much breast cancer incidence.192 The findings of the 2003 study ostensibly apply to all women, yet the authors were especially interested in how their theory might explain why, when fertility rates are higher among African American women, their breast cancer rate is higher, not lower, in contradiction to the estrogen hypothesis. The implication of the study, beyond its scientific claims about the relationship between parity and breast cancer risk, is that pregnancy for young black women is a life-risking enterprise. (The study also feeds the myth of higher fertility rates among African American women; the authors assert that rates were higher at the time of their study, although their data were from 1998. Even if fertility rates were higher for the group of women they studied, it was nevertheless the case that rates in 2003 were much lower than the study’s authors acknowledged.) Indeed, the study cannot account for the present state of affairs: fertility rates are the same between young black and white women, yet breast cancer rates are significantly higher for the former.193 This, then, is the context in which genomics risk discourse takes form, a context in which the intersection of gender and race appears to have particular significance. If the history of racism in medical practice provides any lessons, we can expect that an African American woman at risk will probably not have the same access to cancer prevention techniques as a white woman, including prophylactic surgery. At the same time, the ovaries of black women are considerably more vulnerable if institutional interests lean toward their removal. Genomics, as it turns out, is particularly dependent on the racialization of mutations in order to extend its reach and to maintain its legitimacy in the eyes of funding institutions, a topic I discuss in chapter 4. The population turn in genomics permits the development of screening techniques based largely on skin color and presumed ancestry rather than on family history, the latter being a much more delimiting criterion. Yet BRCA screening has met considerable resistance within the African American community.194 There are a number of observed reasons for this

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to terms with its own legacy of misogyny—a legacy that still informs its method of preventing cancer: prophylactic oophorectomy for any woman for whom the surgery can easily and readily be performed. Indeed, both cancer genomics and gynecology depend on fear of ovarian cancer to deflect critical attention from their conceptual and material practices. The danger of ovarian cancer is real, but it is also relative: surgery does largely reduce risk for ovarian and similar cancers, but it does so at the risk of fatal heart disease, osteoporosis, and brain disorders. The fact that the discourse of ovarian cancer can absorb these other risks is less a matter of its facticity than of its emergence as a mode of legitimation for gynecology in the early twentieth century. Although the surface-level justifications for prophylactic oophorectomy may have changed from the treatment of psychic disorders to the reduction of cancer risk, the justificatory logics are similar, as is the impact on women’s bodies. The recent research on prophylactic oophorectomy has shaken the foundation on which this surgery is routinely and uncritically performed. Yet at the same time, the effectiveness of oophorectomy in reducing risk for BRCA mutation carriers means that the surgery is a crucial mode of legitimation both for gynecology and for genomics. We have seen how, when the risks for BRCA carriers are the same as those for noncarriers, prophylactic oophorectomy remains relatively uncontroversial: the exceptional status for BRCA mutation carriers is possible because of the equation of heredity with fate. To carry a BRCA mutation is, materially speaking, the same as a diagnosis of cancer, for which nothing less than radical surgery is a thinkable mode of action. A rethinking of oophorectomy for women in the general population has entailed resignifying ovaries as agents of health and well-being, and not merely as agents of procreation. But BRCA discourse reverses these critical rhetorical and theoretical developments, first by diseasing ovaries peripherally through the identification of pathological mutations, then by designating motherhood as the only acceptable reason to avoid surgery (albeit within certain age-related constraints). Inherited ovarian cancer discourse is dependent on the dominant, common-sense characteristics of the reproductive body (women have the right to fulfill their procreative desires; those desires ought to be satisfied by the middle of their third decade of life) while it also alters motherhood’s comprehensibility due to the dictates of genomics’ own knowledge claims (because of cancer risk, motherhood must be practiced within a field of constraint). BRCA research, then, is a recuperative project, both for its own ever-changing

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and linguistic displacements (themselves connected to methodological changes) mask the ways in which genomics discourse constructs racial subjects. I consider, for the purposes of the argument here, that genomics’ racializing discourse is ideological insofar as it helps advance and secure state interests—specifically, the disinvestment in antiracism initiatives that would entail fairly significant redistribution of material resources. Indeed, the construction of race in genomics is important in a society that is, according to a number of indices, racist.3 A guiding assumption of the analysis I offer here is that a logic of progression conceals the ways that genomics performs important ideological work without explicit ideological appeals. It is thus an example of what Barbara Fields has described as the ideology of race, the language of which must explain the persistence of oppressive social relations, but that must also change to accommodate the changing face of those social relations. Racial ideology is a vocabulary that “need not and cannot be a duplicate of the one spoken by the rulers.”4 The pathologization of black bodies, through the construction of breast cancer risk, not only affects the medical care and everyday lives of African American women, it also excuses a number of institutional practices that are responsible for the greater chance these women have of dying from breast cancer in the first place. The geneticization of African American women’s breast cancer is, in many ways, the criminalization of black women’s bodies—with testing-related stigmatization and discrimination and the administration of potentially dangerous preventive measures like surgery and drugs—and the decriminalization of the state’s refusal to ameliorate the health effects of racialized social stratification. For clarification purposes, I assume throughout this chapter that “race” is a social designation and that its biological significance inheres in the lived experience of race—the embodiment of social identity—that is in turn related to particular health outcomes. When I employ the terms “black” and “African American,” it is to denote those persons identified and/or self-identified with these terms and who thereby occupy particular positions in a social and economic hierarchy.

The Population Turn in Genomics Those familiar with popular discourse about the Human Genome Project (HGP) have heard Francis Collins and other advocates often count as one of its greatest achievements the production of evidence that all

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for predisposition testing for diseases with some potential for prevention.”9 These findings were confirmed two years later after the researchers worked with communities in the Washington area and recruited 5,000 participants for a follow-up study that examined not only the frequency of the mutation but whether, and to what extent, it increased risk for breast cancer. In 1997 Struewing and coauthors reported that the mutation was found with the same frequency as in their earlier study, and that it was associated with a higher risk for breast cancer. Interestingly, the risk was not as high as with other mutations: women with the 185delAG mutation were estimated to have a lifetime risk for breast cancer of 50 percent, belying the widely held popular belief that BRCA-related risk was not mutation specific.10 In all, three mutations were identified as founder mutations in women of Ashkenazi descent. By 1997 science writers were reporting the identification of many more founder mutations, conveying excitement among researchers that the population turn had firmly taken hold. An article in the Journal of the National Cancer Institute reported: Scientists had hoped the discovery in Ashkenazi Jews (those of Eastern or Central European descent) would help open some doors: to the development of inexpensive tests to check women from this ethnic group for an inherited susceptibility to breast cancer, and to the launch of population-based studies to further understand how BRCA1 mutations cause breast cancer. But the discovery of common mutations among other ethnic groups throws these doors wide open, raising the possibility of genetic tests for populations besides Ashkenazi Jews and expanding the horizons of population-based breast cancer research.11

In the United States, one of those research horizons would include African Americans as genomics researchers set out to describe the existence of founder mutations in black women. The working hypothesis was that if founder mutations existed, like those identified in the Ashkenazim, then perhaps other groups bound by ancestry rather than family would harbor BRCA mutations at a rate warranting targeted research and testing. Three years after the BRCA genes were first described, in a research letter published in the American Journal of Human Genetics, Qing Gao and colleagues made the case for the study of African American breast cancer families. The study of such families, they argued, was justified given the fact that several earlier studies had included black subjects, some of

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the mutations detected are often novel, in the sense that, more often than not, they have not previously been reported—thus demonstrating the need to study African American women for whom extant research data are not necessarily relevant. Third, it demonstrated, as in the Ashkenazi case, the importance of ancestry: if African American women share genetic profiles with women in Africa, might that information be medically useful? And finally, it offered an explanation for differential cancer rates and types of diagnoses among some groups of black US women, especially those stricken with cancer at an early age, statistics that continue to baffle epidemiologists. If studies showed a difference in incidence, mortality, and diagnosis, even when confounding social variables like income were taken into account, might not ancestry help provide a missing piece of the epidemiological puzzle? Could genomics aid in the reduction of health disparities, a high priority research and policy area of federal institutions like the National Institutes of Health, and the National Cancer Institute in particular?

The Rhetorical Problem of Race Generally speaking, geneticists understand “race” to be a social category, but one that nevertheless includes individuals for whom ancestry plays a role in health outcomes. For example, “African American” includes people who can trace their ancestry to West Africa. Heredity research thus identifies genetic markers that link individuals from different racial and ethnic groups from around the globe. The putative goal of BRCA research on people of different ethnic and racial identities is to contribute to medical care tailored to the individual, for whom any number of ancestral markers play a role in disease. Although social categories may be an unavoidable necessity for recruiting study subjects, genomic methodologies are not employed, theoretically, to study race as such. They study populations. Yet BRCA researchers claim to be addressing the problem of health disparities, an epidemiologic phenomenon, not a genomic one. In the 1997 study by Gao’s team, for instance, the researchers made explicit reference to breast cancer statistics that document disparities between white and black women: Among women born and raised in the United States, African American women have a lower risk of breast cancer than Caucasian women. However, the incidence rate of breast cancer in African American women is

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and particular disease outcomes. In breast cancer research, for instance, it is assumed that established risk factors for breast cancer are culturally variant, and thus women who identify themselves or are identified as black or African American are recruited as study subjects (I discuss the problem of the word “culture” and the study of race below in this chapter). Related to this, “health disparities”—a catch-all term21 for observed differences in disease incidence and mortality rates between groups of people defined by race, ethnicity, gender, or socioeconomic status22—presumes that the lived experience of social identity accounts for these differences. Thus, the category African American is medically relevant, insofar as the lived experience of being black in the United States, whether or not one can trace one’s ancestry to Africa, can influence susceptibility to diseases like cancer. That said, epidemiologists studying African American women and breast cancer have nonetheless allowed for—even suggested—genetic explanations for the disparities they observe. The controversy over the 185delAG mutation of BRCA in Ashkenazi women is a case in point, as it opened the door to the subsequent geneticization of breast cancer in racial groups.23 Before the reports of the 185delAG mutation, epidemiologists had claimed that being Jewish was a risk factor for breast cancer.24 At the time, Jewish identity was discussed as a known or established risk factor (sometimes captured by the umbrella term “religion”) by public service organizations like the American Cancer Society (why religion—in particular, Judaism—was thought to increase risk has never been sufficiently explained).25 When, in 1995, geneticists found a link between Ashkenazi ethnicity and BRCA1 and 2 mutations, this risk factor found a biological explanation and, with that, newfound credibility. BRCA research thus provided a discursive site through which risk factors associated with the embodied experience of ethnicity were resignified as manifestations of inherited susceptibility. (In media reporting about the BRCA mutation data, it was at times assumed that the initial 1995 study by Struewing and coauthors had been undertaken with the intent of explaining putatively higher cancer rates among Jewish women).26 At times, epidemiologists seemed as eager to embrace the hereditary explanation of the so-called Jewish risk factor as their geneticist counterparts were. For example, a research team of epidemiologists headed by Kathleen Egan of Harvard University studied Jewish women with a family history of breast cancer and women without such a history. The researchers concluded that risk for Jewish women with a family history of breast cancer was greater than for women in the control group and

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by an increased prevalence of high-grade, hormone receptor-negative tumors[emphasis added].31

The use of the word “race” (or “racial”) in this way may seem surprising given that epidemiology explicitly intends it to be a social category rather than a biological one. A close look at the history, politics, and methodological practices of the field, however, may help explain its implicit, unacknowledged racialism. The inclusion of race in epidemiological research (an aspect of what Steven Epstein calls the “inclusion paradigm”) has a complex history, owing to several interlocking political and economic forces.32 Epidemiology has not, however, successfully elucidated exactly how race plays a role in disease etiology. Janet Shim, for instance, has shown that accepted and routinized epidemiological methods (specifically, the multifactorial model of disease) require that the social reality of race be measured at the individual level. “This kind of devolution,” she writes, “simplifies a complex world into smaller, presumably independent units of observation.”33 Researchers choose those variables “closest” to the observed outcome (disease), and these “typically translate to the direct biological risks or causes of disease and/or to the lifestyles or behaviours addressable at the individual level.”34 Race, in effect, becomes a black box, allowing epidemiologists the political luxury of claiming to explain health disparities even though their data do not shed light on what it actually means for race to explain health—it is, in practice, merely assumed. Indeed, “adjusting at the individual level for an effect that occurs causally at the society level cannot logically produce a meaningful model of disease etiology, no matter how refined the measures.”35 What the multifactorial model does accomplish is the association of race with observable, isolatable, biological characteristics of the racially classified person, decontextualized from the array of factors associated with lived experience. For example, social isolation, a manifestation of structural racism, is one way in which race increases risk for breast cancer.36 But to study the effects of social isolation, researchers measure glucocortisoid levels in individual women. These physiological changes in the body do not, in and of themselves, explain the complex connections between racism, social isolation, and one’s embodied experience of these social relations. The examination of these bodily changes opens up the possibility—and a likely one as this knowledge makes its way into public health and medical practice—of correcting for elevated glucocorisoid levels at the individual level.37 In turn, the complex processes by which race

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Shared observations of disparities in health . . . do not necessarily translate to common understandings of cause; it is for this reason theory is key. Consider only centuries of debate in the US over the poor health of black Americans. In the 1830s and 1840s, contrary schools of thought ask: is it because blacks are intrinsically inferior to whites?—the majority view, or because they are enslaved?—as argued by Dr. James McCune Smith (1811–1865) and Dr. James S Rock (1825–1866), two of the country’s first credentialed African American physicians. In contemporary parlance, the questions become: do the causes lie in bad genes?, bad behaviours?, or accumulations of bad living and working conditions born of egregious social policies, past and present? The fundamental tension, then and now, is between theories that seek causes of social inequalities in health in innate versus imposed, or individual versus societal, characteristics. Yet, despite the key role of theory, explicit or implicit, in shaping what it is we see—or do not see, what we deem knowable—or irrelevant, and what we consider feasible—or insoluble, literature articulating the theoretical frameworks informing research and debates in social epidemiology—and epidemiology broadly—is sparse.41

Despite these serious, arguably crippling criticisms of health disparities research and the epidemiological methods it typically employs, genomics’ incursion into this field of inquiry is not simply epidemiology’s latent biologism taken to its logical conclusion. Epidemiology encompasses a diverse field of practitioners, and many of its critics, like Krieger, hail from within the field.42 The result is that the use of ethnic and racial categories is routinely contested and debated, and they therefore remain conceptually in flux. The so-called Jewish risk factor, for instance, was contested at the time of the first BRCA report on the relevance of Ashkenazi ancestry.43 Significantly, when that report was published, it seemed to provide evidence for those eager to define Jewish men and women as a biological Other. Public discourse about the relationship between BRCA and ancestry reduced the complex interplay of embodied life and health to genes, a metonymical substitution of part of an ethnic group (the Ashkenazi) for the entire ethnic group (Jews). The 185delAG mutation was commonly referred to in media reports as “the Jewish breast cancer gene” (a Buffalo News article went so far as to claim that it resides “solely” in Jews). This episode demonstrates how an epidemiological risk factor, one that

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more generally.50 Moreover, “the 943ins10 allele has not been observed in any patients with breast cancer who identify their ancestry as solely European.”51 The researchers argued: The migration patterns of African Americans and, hence, the current areas of residence of African American families, may explain the difference, among clinical centers, in the prevalence of the mutation. To determine, among African American women, the proportion of inherited breast or ovarian cancer attributable to BRCA1 943ins10, we would like to encourage testing for this mutation among African American breast and ovarian cancer52 patients from various regions of the United States. Given the increasing incidence of and higher mortality from breast cancer among African American women, it would be useful to obtain as much information as possible about the roles of BRCA1 and BRCA2 in this population.53

The authors of this study were careful to employ the term “population”; indeed, founder mutations, by definition, are material artifacts of ancestry, not race. And ancestry, unlike race, is not a geographically bound concept. So, for example, the 943ins10 mutation is present in individuals who cannot trace their ancestry back to Africa, just as the 185delAG mutation has been found in people residing all over the world. Founder mutation research casts its testing net far and wide, identifying specific alleles of genes in people from around the globe in order to trace their evolutionary history. Thus emerge particular meanings of “population.” Founder mutation research has not, to date, resulted in the identification of mutations that would justify targeted screening of women for whom West African ancestry can be confirmed. Nevertheless, researchers have discovered a novel way of circumventing this apparent genetic dead end: the similarity of breast cancer itself in African American and West African women. Breast cancer, in other words, has become the observable phenotype of a suspected underlying genotype. Two studies are representative of the belief that the morphological characteristics of breast tumors imply an ancestral connection between these two groups of women. In the first study, seventy young Nigerian women of African ancestry (all but four were diagnosed with breast cancer at or under the age of forty) were tested for BRCA1 and BRCA2 mutations.54 The sample was ostensibly chosen because, they say, African women are more likely to be diagnosed with breast cancer at an earlier age

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American women. The conclusion of these authors, in fact, is that continued genetic testing of black women here and abroad is both medically and scientifically justified. One consequence of presumed shared ancestry is that it geneticizes these breast cancers by drawing attention away from other reasons why these two groups of women suffer from similar tumors (and why, in many cases, they do not). Indeed, the very design of these studies is conceptually and methodologically limited insofar as comparisons of African and African American women overlook and/or ignore important differences that may exist within these arbitrarily defined groups. (Related to this is the problem of relying too much on study designs that compare black and white women, either here or in other countries.)59 These BRCA studies tell us nothing about differences among black women—that is, how their risks vary due to the complexities of embodied experience. Mapping the African heritage of breast cancer seems to hold more significance for BRCA researchers than ascertaining what, if any, medical relevance there is in doing so. Yet very real differences exist between black American women and black West African women. Breast cancer is much more common in the United States than in West Africa, and this itself raises a number of questions regarding the role of environmental factors in breast cancer trends. More important, the demographics of breast cancer, both here and in west Africa, are ever-changing, shifts that cannot be explained by evolutionary processes that take hundreds, if not thousands, of years to unfold. And not all black women, of course, are diagnosed with the type of breast cancer described in these studies. Nor are all white women excluded from this particular risk profile. One essay rightly concluded: Race and ancestry are confounded both by genetic heterogeneity within groups and by the widespread mixing of previously isolated populations. The assignment of a racial classification to an individual hides the biological information that is needed for intelligent therapeutic and diagnostic decisions. A person classified as “black” or “Hispanic” by social convention could have any mixture of ancestries, as defined by continent of origin. Confusing race and ancestry could be potentially devastating for medical practice.60

Here the case of sickle cell anemia and sickle cell trait is instructive: “If sickle-cell disease is suspected, then the correct diagnostic approach

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Interestingly, the near-exclusive attention to African ancestry belies the lack of evidence of founder effects66 on breast cancer risk in black women. More important, the medical relevance of ancestry depends, for obvious reasons, on its being a decisive factor in recommendations for prevention. Yet by some accounts, approximately 35 percent of African American women cannot trace their ancestry to West Africa. Complicating this further is the fact that “by some estimates more than three quarters of Americans who identify themselves as black or African American have a blood relative who identifies themselves as white or Caucasian.”67 But the literature on founder mutations often ignores the very real possibility that the “African” founder mutation 943ins10 could be detected in “white” women. According to one data set published in 2003, over sixty BRCA1 mutations had been detected in African American and African families as well as in families with no reported African ancestry. One of these mutations is the 943ins10 founder mutation of the BRCA1 gene.68 To better illustrate why the privileging of African ancestry is a unique and significant development, consider, for the purposes of comparison, the discourse of white breast cancer. According to the epidemiological data cited by BRCA researchers, compared to black women, white women in the United States are more likely to get breast cancer (except women under the age of thirty); are less likely to die from breast cancer; and are more likely to be diagnosed with less aggressive, more treatable tumors. Arguably, this epidemiological profile of breast cancer would suggest that ancestry might explain these breast cancers—in this case, European ancestry. But white women are not described in this manner. As of 2008, the word “white” or “Caucasian” has never appeared in a title of a BRCA research article, as there has been no attempt to explain “white” or “Caucasian” breast cancer as “white.”69 No studies exist that racially group white women in the United States and white women in Europe. Rather, we have studies on founder mutations linking women within or across particular nationstates.70 (Whether or not one can really say there is a Finnish or Spanish BRCA mutation is beside the point; the attempt to do just that demonstrates that women can be grouped any number of ways. What the critic must do is consider how these choices are made and why they matter.) The de facto assumption is that white women are a genetically diverse population formed from multiple ancestral lines, any of which may or may not play a role in breast cancer risk.71 As a result, European ancestry was complicated early on with the identification of mutations linked to the Ashkenazim. For white women, then, significant family history, personal

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Hispanic background. At least one study has found a suspected founder mutation in people reporting Hispanic ancestry. In a caveat, the authors wrote that although “Latino” is a term employed the US Census and is more of an “ethnic” or “cultural” designation, they purposefully employed “Hispanic” as a way to understand the intersection of this social group’s particular evolutionary history and breast cancer risk.77 Although this may very well have the effect, at some point, of homogenizing, or racializing the identity “Hispanic,” so far no one part of this group’s ancestral history has been privileged over another. Instead, geneticists have engaged in a complex, nuanced examination of the evolutionary history and dispersed geographical locations of their Hispanic study subjects. One such example is the use of the term “mestizo.” Here, researchers are acknowledging the existence of multiple ancestries and an attendant genetic admixture rather than privileging continent of origin, as they do in the case of African American women. The suspected BRCA1 founder mutation del (ex 9-12) that is prevalent among study subjects identifying themselves as Hispanic has also, as it turns out, been reported in persons who identify themselves as African American and Native American. The mutation’s investigators conclude that because BRCA mutations may account for a “higher proportion of the breast cancers in young Hispanic women,” this group is “analogous” to the Ashkenazim.78 Notably, they do not invoke young African American women for comparison purposes. What I have described is just one way in which BRCA research racializes breast cancer. In the next section, I describe another, closely related discursive development. I argue that in the absence of founder mutations, it has not been scientifically possible to group women together by way of specific mutations they all share. Black women in the United States and in West Africa are not, as it turns out, linked by specific, shared genetic markers; they are linked by virtue of their genetic diversity—in this case, the diversity of BRCA variants identified by mutation databases. The result is the racial demarcation of women based on relative genetic diversity.

“Diversity” as Racial Signifier Before exploring how genetic diversity acts as a racial signifier, it is first necessary to understand its origins in debates about race and science, in particular how it has grounded some of the most powerful and effective scientific challenges to the race concept. Beginning with naturalists in the eighteenth century, race was principally used to make sense of observed

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patterns of human genetic diversity are compatible with categories of race, the latter defined as the primary continent of origin.85 There is a growing debate as to whether or not a genetically inferred primary continent of origin demonstrates a material reality to socially constructed racial categories—what Jonathan Marks, a critic of the use of race, has termed the “gene pool residual” understanding of race.86 For many researchers, the answer is yes, which has raised the further question of whether the label “African American” can be a proxy or surrogate for African ancestry, a question reaching lay audiences with the March 2005 publication of an opinion piece by the biologist Armand Leroi in the New York Times.87 Leroi claimed that race is in fact a useful proxy or shorthand for human genetic diversity, dismissed the methodology behind Lewontin’s 1972 essay as outdated, and cited several articles demonstrating a near correspondence between racial identity and genetic cluster groupings. Cluster analysis, in which researchers sort study subjects into genetically similar subgroupings, can be performed with or without knowledge of individual racial or ethnic identity. The fact that it can be done without such knowledge has led some researchers to conclude that racial identity should never be a part of the geneticist’s research methodology.88 For others, including the geneticist Neil Risch, it is too soon to jettison the use of racial and ethnic labels. Although both sides of the debate share the goal of individualized, whole-genome analysis, in the short term, these researchers suggest, proxies are both technologically and economically necessary.89 Moreover, they argue, a colorblind method would impede researchers’ attempts to improve minority health. Failure to acknowledge the race or ethnicity of research subjects makes it difficult to take into consideration nongenetic variables connected with lived experience—variables that can affect health outcomes. According to this reasoning, geneticists have an obligation to study race in both its social and biological dimensions: Studies using genetic clusters instead of racial/ethnic labels are likely to simply reproduce racial/ethnic differences which may or may not be genetic. On the other hand, in the absence of racial/ethnic information, it is tempting to attribute any observed difference between derived genetic clusters to a genetic etiology. Therefore, researchers performing studies without racial/ethnic labels should be wary of characterizing difference between genetically defined clusters as genetic in origin, since social, cultural, economic, behavioral, and other environmental factors may result in extreme confounding.90

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of the project, documenting over a million SNPs thought to be common in humans, will allow researchers to more easily pursue case control and exploratory studies in order to both determine the degree of risk associated with suspected pathological alleles and to locate more regions linked to disease onset.94 The guiding principle of the HapMap project is the biomedical significance of diversity, yet the sampling methodology suggests that diversity is important only insofar as it marks off differences among the continents. Thus the HapMap consortium, while recognizing that no one population would be necessary for inclusion in order to map common SNPs, sampled a number of populations that nevertheless correlate with common understandings of race.95 Like the cluster studies I describe above, the HapMap project demonstrates the essential paradox of genetic diversity in a culture structured by racialism: diversity, more often than not, serves to reify group boundaries, not break them down. A close examination of BRCA discourse helps elucidate how this reification occurs. It was perhaps inevitable that diversity would be a topic of interest for BRCA investigators in the wake of the population turn. As the research progressed and more and more study subjects were tested (although recruitment has remained quite low), it became clear that not only did a statistically significant number of black women test positive for BRCA mutations, but the tests produced much different data than those found in other populations. In one study, for example, nineteen BRCA variations were detected in forty-three black families, as opposed to just nine variations in seventy-eight white families.96 Many of these genetic variants were not reported in other groups. (This is why African American women are more likely to test positive for variations for which no clinical research is available.) The range of diverse BRCA alleles—as well as their novelty—has not disproved the anachronistic meaning of race so much as provided new material evidence for it. As the data about BRCA diversity have accumulated, the language of the unique and distinct genetic profile has proliferated. Consider the following excerpts: Our data and those of other groups support the presence of a diverse spectrum of BRCA1 and BRCA2 mutations and sequence variations unique to Blacks of African descent.97 The spectrum of mutations we observed in African Americans is vastly different from what we observed in individuals of European descent.98

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the existence of race on the grounds that no set of unique genetic markers could be found to group persons together, unequivocally, under the umbrella of race. But although there is greater diversity within races than between them, it is still the case that the greatest degree of diversity can be found among individuals of African descent. Follow-up studies to Lewontin, for instance, have shown that the most diversity is found in Africa and African Americans due to genetic admixture and the intersection of multiple ancestral lines.103 So greater diversity signifies African race, and lesser diversity characterizes other races, at least according to those scientists motivated to find ways to prove both the existence and medical relevance of diversity. In practice, BRCA alleles labeled “unique” to one group of people have subsequently been reported in other groups. In a study of BRCA mutations in German subjects, for instance, a mutation detected in a “white” subject happened to be the same one that Gao and coauthors had previously labeled “unique” to blacks. The term “unique,” then, does not really mean exclusive. Even if “unique” in this context means “common to,” relative diversity, as I have shown, nevertheless distinguishes blacks and whites and thus constitutes the former as a race. Future studies of African Americans are likely to reveal many more BRCA variations than will be found in whites. Gene frequency research, along with research that privileges African ancestry by drawing parallels between African and African American women, is unlikely to yield nuanced studies of African Americans as an ethnic population for which African ancestry is just one part of a complicated evolutionary history that may or may not be medically important. These genetic discoveries are more than just evidence of the vagaries of genomics research; in a larger social context in which scientists and the lay public alike still believe in a biological basis for race, the use of words like “unique” and “distinct” matter, both in terms of validating popular beliefs and of discursively constituting racial subjects anew. “Admittedly, racial categorization is not the same as racism,” says Jacqueline Stevens, “but racial categorization never happens without also producing racial hierarchies.”104 A significant percentage of African American women can trace their ancestral roots to West Africa; they thus constitute a “population” in the same way that women of Ashkenazi descent do. However, lay understandings of population often displace more specialized ones in popular and scientific discourse alike. Thus, the mutation 185delAG came to be known as the “Jewish” mutation even though it was detected in a variety of

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among young white women, and have been so for some time. As Krieger has observed, “combine relatively high incidence and relatively high mortality, and the net result is that US Black women have among the highest breast cancer mortality rates in the world.”108 Viewed historically, breast cancer mortality rates among black women in the United States evince a disturbing pattern. Between 1973 and 1990, incidence in black women under fifty increased by over 16 percent, while the increase for white women in this age group increased by 6 percent.109 Between 1969 and 1997, the age-adjusted death rate for white women dropped 15 percent, while it increased by 22 percent for African American women.110 Rates are very high among older black women. Gross rates of breast cancer in women younger than fifty between 1992 and 1997 were actually lower for black than for white women, although adjusted for age they were slightly higher. These trends defy a genetic explanation: “beyond the clinical trials, epidemiologic assessment of the US population suggests biologic/genetic differences may have been overemphasized. Often unappreciated is the fact that black-white mortality was very similar in the 1970s and the disparity in mortality rate has grown every year from 1981 onward.”111 The cancer community rallied around these rates, evidenced in part by a major conference in 2003 devoted to the subject of health disparities and culminating in a special issue of the Journal of the National Cancer Institute. “Race” is an operative word in this discourse, and deservedly so, as women who identify themselves or are identified by others as black or African American arguably experience life events differently than women classified otherwise. Race is a determining factor, for instance, in relative experiences of poverty and discrimination, which in turn can affect nutrition, stress, access to preventive care, access to palliative care, and overall well-being—all essential to whether a woman develops disease and, if she does, can survive it. This historical trajectory is material evidence of the social dimensions of black-white breast cancer rates. The field of health disparities research112 emerged as a direct response to the persistent, often startling statistics charting an ever-widening gap between blacks and whites in breast cancer incidence and mortality. As I argued above, epidemiologists and geneticists alike have questioned whether epidemiology possesses the methodological tools necessary to fully explain differences in breast cancer rates. Yet the claim that genomics must step in to explain these differences implicitly assumes that epidemiology is, paradoxically, both

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Perhaps the most striking finding that emerges from the analyses of social environmental influences is the graded and continuous nature of the association between income and mortality, with differences persisting well into the middle-class range on incomes. The fact that socioeconomic differences in health are not confined to segments of the population that are materially deprived in the conventional sense suggests strongly that socioeconomic differences are not simply a function of absolute poverty. Moreover, because causes of death that are purportedly not amenable to medical care show socioeconomic gradients similar to those of potentially treatable causes, differential access to health care programs and services cannot be solely responsible for these differentials in health. Finally, because the gradient in morbidity and mortality persists even between middle class and well-to-do men and women, and even in societies in which material conditions are very good, it seems unlikely that gradients are due solely to material circumstances per se.114

“Race” confounds epidemiological data, not because underlying genetic/biologic variables are at work, but because “race” is not yet adequately theorized. Specifically, researchers must think creatively about how racial discrimination structures the everyday life of African Americans of all socioeconomic status designations—what feminist studies scholars would say is the need to understand the intersection of oppressions in the context of health. The study of racial differences in health must consider their effect beyond presumed access to resources and colorblind assessments of socioeconomic status. Lewontin astutely observed that “asbestos and cotton lint fibers are not the causes of cancer. They are the agents of social causes, of social formations that determine the nature of our productive and consumptive lives, and in the end it is only through changes in those social forces that we can get to the root of problems of health. The transfer of causal power from social relations into inanimate agents that then seem to have a power and life of their own is one of the major mystifications of science and its ideologies.” Shifting the focus to lived experience can return causal power to the social sphere. One model for studying race as lived experience as the outcome of embodiment, not heredity, is the “ecosocial” model put forward by Krieger. Focused on the guiding question of “who and what drives current and changing patterns of social inequalities in health,” ecosocial theories combine the concerns and methods of political economy

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proffered the theory that breast cancer mortality among black women is inextricably linked to social and economic environments. Their work, situated at the Center for Interdisciplinary Health Disparities Research, is part of a consortium of mostly publicly funded university-based centers, collectively called the Centers for Population Health and Health Disparities (CPHHD).120 In 2007, the consortium published a progress report, titled “Cells to Society: Overcoming Health Disparities,” in which they wrote: The mapping of the human genome provided an important platform for addressing the causes of cancer disparities in individuals and populations. New personalized medicine technologies also promise to help many individuals with cancer. However, while such approaches are essential, they are insufficient on their own for the development of an effective and efficient long-term strategy for gaining knowledge and preventing disease at the population level. Indeed, the explanations for disease occurrence in a population may be quite different from the causes of interindividual differences in disease occurrence.121

CPHHD research is “vertically oriented, starts at the top with race, poverty, disruption, and neighborhood crime; moves to isolation, acquired vigilance, and depression; then to stress-hormone dynamics; and finally to cell survival and tumor development.”122 The consortium’s researchers “found that social isolation, vigilance, and depression were highly correlated and represent facets of a ‘psychosocial suite’ that represents how the social environment gets ‘under the skin’ to alter the body’s ability to repair cells.”123 One hypothesis in particular that has captured their attention is the role of glucocortisoids in race-specific stress and the connection of that role to cancer development. Activation of glucocorticoid receptors sets off a chain reaction of biological responses that ultimately helps cancer cells survive. Thus, “higher reactivity to stress may predict earlier tumor development through heightened secretion of glucocortisoids.”124 Another ecosocial hypothesis is that black women are more likely to be exposed to a certain class of chemicals known as organochlorines (OCCs), which increase breast cancer risk. The theory is that OCCs, such as the pesticide DDT and polychlorinated biphenyls (PCBs, now-banned chemicals used in the manufacture of electronics), are estrogenic and thus increase breast cancer risk (the effect being similar to reproductive

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[A racial project] is simultaneously an interpretation, representation, or explanation of racial dynamics, and an effort to reorganize and redistribute resources along particular racial lines. Racial projects connect what race means in a particular discursive practice and the ways in which both social structures and everyday experiences are racially organized, based upon that meaning.132

Constructions of race are crucial to the successful operation of a racial project insofar as they undergird institutional practices and policies. In the 1950s, for example, unwed black mothers were blamed for soaking up precious economic resources and exacerbating the perceived economic insecurity of whites. In this way, argues Rickie Solinger, reproductive capacity justified both status quo economic arrangements as well as policies that would concentrate wealth even more among white people. Crucial to this discourse was the belief that these black mothers were simply fulfilling a biological imperative bestowed on them at birth. Black female sexuality, implicitly taken to be an inborn trait, pervaded political discourse at the time. Even when “culture” replaced “biology” during brief periods of progressive social form, argues Solinger, it was really just a “dignified cover for biological racism.”133 In this chapter I have discussed what I call progressive epidemiology’s willingness and ability to reflectively consider how science inadvertently reifies race. This work has made it possible to show that structural and institutional racism results in extreme suffering. Indeed, it kills. Yet health disparities scholars—who hail from multiple scientific disciplines, and many of whom are ardent critics of the race concept—remain deeply invested in biological studies of health disparities. It is, of course, reasonable to expect them to be so. Ironically, insofar as these epidemiologists compel intervention at the social level, they may undermine the necessity of their work over the long term. Elevated glucocortisoid and OCC levels are not the causes of breast cancer—they are, to borrow Lewontin’s phrase, agents of social causes. To intervene at the level of social causes, then, is to move beyond epidemiology’s focus on illuminating proximate causes and into the arena of social movement and policy change. Research is surely required to substantiate the importance of such interventions. But that research may need to come from the humanities as well as the social sciences (in the interest of full disclosure, I consider myself a scholar working in the humanities). Making the case for the relevance of historical methodology for understanding health disparities, and specifically

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Fujimura and Ramya Rajagopalan have also concluded that race seems to be so firmly entrenched in the mental habits of scientists that methodological improvements are insufficient in dismantling the latent belief in, and ultimate materialization of, race.139 (In an interesting twist, the profit motive may serve as a bulwark against racialization. In a 2009 study sponsored by the company Myriad Genetics and published in Cancer, the authors concluded that all high-risk women are candidates for BRCA testing regardless of racial or ethnic identity.140 Although as Epstein points out,141 pharmaceutical companies will continue, for the foreseeable future, to create niche racialized markets.) Proof of the persistence of race supports Stevens’s proposal that the National Institutes of Health refuse to fund any genetics study that purports to explain health disparities unless “statistically significant disparities between groups exist and [the] description of these will yield clear benefits for public health.”142 This would prove a very high bar and would result in drastic reductions in current funding levels. Defunding genetics research is a different type of material change than, say, switching software from structure to EIGENSTRAT to determine gene frequencies of populations. It could effect, rather, a change in the external material conditions and social structures (much like the antiracism initiatives I listed above) that are the reason why racial ideology persists. I have no doubt that that the scientists and race critics I have cited would disagree. The Chicago study on social isolation, for example, understood hormone levels to be products of gene expression; Krieger’s ecosocial model is premised on the integration of social and biological research; and Fausto-Sterling, after a thorough treatment of the persistence of race and why genomics research diverts attention away from the link between racism and disease, nevertheless concludes: “We need, instead, to develop the habit of thinking about genes as part of gene-environment systems, operating within networks that produce new physiologies in response to social conditions.”143 Indeed, what I have not yet considered is whether genomics permits us to consider “gene-environment” interactions, a dialectical relation that does not, in and of itself, privilege one part over the other and that has greater explanatory power than either genomics or epidemiology alone. Gene-environment interaction is embraced by a great many stakeholders in health disparities research initiatives. I have assumed thus far that genomics functions as a racial project of sorts, insofar as its understanding of race—as a diachronic, natural, immutable trait—undermines the

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contrast to the situation in the European Union, which is much more likely to require safety testing before commercialization. Related to this is the widely accepted belief in the United States that it is up to consumers to force industry to replace toxic chemicals with safer alternatives. Lax environmental regulations, it is believed, can be circumvented through consumer-driven creation of markets for safer products. An ethos of individualized, privatized fields of action ignores and thereby exacerbates the class, race, and gender dimensions of health disparities. Environmental justice activists have shown, for example, that dirty industries are concentrated in poor communities of color.5 Citing evidence that dates back to the early 1970s, Robert Bullard6 notes that a strong correlation exists between the conditions associated with political and economic disadvantage and disease.7 An early study of the 1,000 residents (all of whom were black) of Triana, Alabama—a community contaminated with DDT and PCBs—revealed the highest human levels of DDT ever recorded.8 Stress, lack of access to healthy foods, social isolation, and other factors make residents in such communities more vulnerable to diseases associated with exposure to environmental contaminants. Moreover, safer alternatives to many products are not available for purchase in these areas or are simply cost-prohibitive. In short, these communities are not well served by the pervasive and celebrated expansion of the market into public health and medicine, an expansion that is incompatible with the notion that social change, much of which can be effected at the policy level, is needed to correct the current state of affairs. Although much attention has been paid in recent years to the problem of health disparities—for example, differences in the incidence of and mortality from breast cancer between white and black women—research in this field does not necessarily draw attention to the limits of the current regulatory structure and its increasing reliance on market principles. In part, this is because of a latent biologism that health disparities scholars can and do rely on. Biologism has, historically, worked in the service of free-market norms, explaining the social order of things as the natural order of things, belying the need to correct for the maldistribution of resources. Some health disparities research contributes to the biologism of race in particular and, by extension, its connection to class. As I argued in the last chapter, drawing on the work of Janet Shim and Merlin Chowkwanyun, when race is seen as a risk factor in epidemiological research, it remains insufficiently explained at best, susceptible to reification at worst. A pervasive lack of historical perspective in health disparities research

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that tend to be inherited unchanged. Because people share haplotypes, researchers can compare and contrast the haplotypes shared by those with a particular disease and by those without it. The identification of molecular differences in the haplotypes can then set the stage for determining just what role genetic variation plays in disease onset and resistance.12 Environmental genomics promises to elucidate the molecular mechanisms of variable risk in populations—the so-called gene-environment model. Environmental health advocates embrace this model, because they believe explanations of how environmental agents interact with the genome in disease etiology can ground arguments for the ban or restricted use of individual chemicals or classes of chemicals. For example, Devra Davis, an epidemiologist and a fierce proponent of regulatory reform, has often invoked gene-environment interaction to demonstrate the causal links between exposure and disease. Some environmental breast cancer organizations, including those devoted to research and advocacy, take gene-environment research to be an essential part of an overall strategy to raise awareness about and politicize the connections between this disease and pollution. A newsletter of the Silent Spring Institute, for instance, included a discussion of research on PCB exposure among genetically susceptible persons and the risk of breast cancer.13 In short, environmental health researchers embrace the gene-environment model, believing that genetic variants are an important causal factor in complex biological processes. And policymakers believe that knowledge of genetic variation helps make prevention more accurate and cost-effective against a backdrop of scarce and dwindling resources for health care and public health. In 1999 Steven Coughlin, a researcher at the CDC, explained this reasoning: “In the near future, the identification of genotype through genetic screening might allow for the identification of persons truly at high risk for an illness, targeted medical interventions, and improved allocation of health care resources” (emphasis added).14 The newfound popularity of the gene-environment model is reflected in several well-funded federal initiatives. At the CDC, the National Office of Public Health Genomics15 integrates developments in genomics with the CDC’s public health mandate. Calling attention to the importance of gene-environment interaction in health and disease, in 2001 the office’s director, Muin J. Khoury, stated that “the public health impact of the human genome revolution is truly staggering.” Common diseases and those responsible for “nine of the top 10 leading causes of death,” he wrote, “have genetic components resulting from the interaction of genetic

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to encourage, and simplify, research linking specific diseases to gene variants. Taking a more targeted approach, the Environmental Genomics Group, also at the NIEHS, “works to characterize the role of genetic variation in human toxicological responses, especially to discover human alleles that modify responses to exposure and to investigate how such alleles affect risk in exposed people. This information is useful in determining appropriate variability parameters in human risk estimation models, in identifying at-risk individuals and in devising disease-prevention strategies.”21 Whether these articulations of gene-environment interaction will lead to broad-based environmental regulatory reform depends on the ontological and epistemological status of the terms themselves. From a dialectical perspective,22 DNA interacts with cellular components (such as proteins) in a mutually constituting process that, although limited by developmental possibilities, nevertheless allows for much contingency and variability. In this model, common terms associated with DNA, like “replicate,” “code,” and even “messenger”—as in messenger RNA, which by some accounts serves merely as a conduit for translation—no longer make sense. No one component of the biological organism may be said to have an identity or essence prior to its relational activity with other components. In contrast, in the unidirectional model, best represented by Francis Crick’s central dogma hypothesis, DNA is not dependent on environmental variables for its expression. Genes and environments interact with each other without ever fundamentally altering each other’s substance. The genome’s identity is understood to be stable over time, exerting its influence unilaterally. This understanding of the genome reduces the agency (and, by extension, the importance) of the material and natural environment. And it is a model that renders change at the production and social levels increasingly unthinkable. Like their eugenicist predecessors, postwar molecularists such as Crick believed that knowledge of the genome gave scientists unprecedented power to change it—genetic engineering became the sought-after scene of human ingenuity.23 Although this hubris is largely absent from genomics discourse today,24 the antihistoricism and antimaterialism of the central dogma (and more recently of the HGP; see chapter 2 for an elaboration of this point) has nevertheless been reiterated in the rhetorical work of the gene-environment model, one that bears the conceptual and ideological traces of the central dogma and its privileging of nature over nurture as the field of action. Environmental genomics assumes, first, that pollution is an unavoidable

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Within this context, environmental genomics presents genetic subtyping of the population as the way to circumvent the need for broad-based environmental health initiatives. Yet the argument presumes that genetic analysis reveals more meaningful information than that produced by epidemiological methods. Genomic methods, however, do not reveal underlying categories of susceptibility so much as they define these categories in advance. And as is the case with genetic testing in general, there is a great deal of uncertainty around the interpretation of the results beyond simply placing someone in one of these predetermined subsets. The genetic test cannot specify the agent of action (for example, employer, employee, or policymaker) or say whether or not the person tested will actually succumb to disease if exposed. More important, genomics cannot say for certain whether or not those persons receiving negative results (that is, those who test negative for an allele connected to disease susceptibility) are really safe. Some of the most dangerous chemicals would, presumably, remain in use given the logic of the genomics model, provided those who show genetic evidence of susceptibility are removed from the exposure site. Take the example of benzene, one of the most dangerous chemicals in use today. Research has documented its harmful effects at exposures well below legal levels. We know this in part because of knowledge regarding the effects of benzene exposure at the molecular level.29 The connection between genetic variants and the metabolism of benzene,30 however, weakens the incentive to remove benzene from industrial sites,31 thus permitting the exposure of most workers (that is, those who do not possess the genetic variants that we know affect metabolism). In a 2010 research article on benzene, for example, Qing Lan and colleagues admit to the “ubiquity” of benzene pollution and its economic importance to industry, thus providing a rationale for allowing the use of a chemical that was at one point deemed too dangerous at any level of exposure.32 This logic is not confined to research on just one chemical—it informs the very federal programs that are setting the stage for a genomics-inflected approach to environmental and occupation health. “Many diseases are the outcome of a complex inter-relationship between multiple genetic and environmental factors,” according to the NIEHS. “Research suggests that individual susceptibility is influenced more by certain genes than by exposure to environmental agents.”33 And for those subject to testing, history does not offer many examples to recommend it. The intersection of undue industry influence and structural racism led to widespread discrimination in employment and

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and Collins describe as the “individual and dynamic extent of the exposure and its impact on fundamental biological processes.”39 These markers in turn isolate the field of action, a pragmatic need of public health and medicine alike. According to Weis and coauthors, “the assessment of exposure and risk should focus on understanding the biologic processes of human disease by defining markers that represent and link events, both genetic and environmental, in the exposure-disease relationship.”40 These novel methodologies will, in turn, permit early warnings or diagnoses and chart a path for prevention and treatment.41 The privatization of risk is not unique to the encroachment of genomics into environmental health.42 Developing ways to ascertain evidence that environmental exposures have occurred (for example, by detecting the formation of DNA adducts, places where nucleotides have bonded with chemical agents) arguably narrows the visual field to the body and invites highly personalized interventions. Nevertheless, explaining this biological activity with a hereditarian lexicon involves a different sort of biopolitics. Environmentally induced changes are somatic; susceptibility is an inborn trait. The heredity paradigm holds that genetic variants are insular entities, wielding their influence unidirectionally, unaltered by the biological context. Schwartz and Collins, for example, write that the “assessment of environmental contributions is much more difficult than for genetic ones. The genome of an individual represents a bounded set of information, remains basically stable over time, and is very well suited to multiple analytical approaches.”43 In other words, susceptibility is a biological state that a person inherits but cannot acquire; the genome is, for all intents and purposes, immune from the effects of embodied existence. Whereas epidemiology theoretically leaves open the possibility that disease is the outcome of historical, political, and economic forces, the very idea of hereditary susceptibility renders the historical-embodiment perspective, exemplified by the approaches of social epistemology and political economy of health, ineffective, even counterproductive. Schwartz and Collins, for instance, point out that environmental exposures are difficult to isolate but genes are not—genetic screening thus replaces the methodologically, politically, and socially difficult process of gaining access to historical records, data about toxic releases (which often take social movements and acts of legislation to procure), medical records, and the input of the public, all of which are needed if the goal is to prevent or remediate environmentally induced disease. Although, paradoxically, these environmental genomics advocates call for the transformation of environments, not genes,44 an

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ways—revealing that state actions are not necessarily designed to maximize the health of all.49 For instance, although the stated telos of genomics research is individualized medicine, short-term reliance on racial categories has produced new routes to racialization. The most common methodology employed by environmental genomics programs relies on maps of population-based genetic variation. The HapMap is often cited—for example, by Schwartz and Collins—as a model for mapping SNPs of interest; in fact, it has been recommended that data from the HapMap be used, in the short term, to connect public health burdens with specific genetic alleles.50 Recall from chapter 4 that the HapMap project, despite its stated purpose in mapping genetic variation across the human genome, nevertheless selected as its representative sample people identified as members of geographically isolated groups, groups looking suspiciously like “races,” anachronistically defined. The EGP employed a similar methodology. Its GeneSNPs Database is based on ninety-five individuals “representing the ethnic diversity found in the United States.” Although an improvement over the four “races” implicitly employed by the HapMap designers, the database nevertheless opens the door to associations between disease and ethnicity, associations that will most likely not include whites, the dominant group. An additional way in which racial and ethnic groups will be profiled will be by first defining and targeting particular disease groups using the tools of environmental epidemiology. According to Weis and coauthors, “new study populations can be identified using global screening tools such as GIS-based [geographic information system–based] technologies to identify specific sub-populations with unusually high rates of the disease or potentially elevated exposures for the disease.”51 The obligatory consideration of race,52 however, makes it likely that the association between geography and race will ultimately be geneticized.53 GIS defines a disease community by virtue of the inhabitants’ location—understood as the multilayered confluence of a variety of social demographic variables, such as education, income, and socioeconomic status—in order for researchers to determine the role and influence of confounding variables. Yet what happens when population alleles are included in the analysis? In a 2005 essay on GIS, lead, and children’s health, Marie Miranda and Dana Dolinoy describe how GIS can be used not only to locate high-risk populations but also to incorporate gene-environmental models of lead levels in children’s blood. Race, they say, “consistently remains as an independent explanatory variable for elevated blood lead

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lifestyle paradigm has been under fire from progressive researchers like Steingraber for its implied assumption that individual free will can trump the range of social factors that overdetermine the degree to which one is exposed to carcinogens—what Lewontin has described as “the social formations that determine the nature of our productive and consumptive lives.” The lifestyle paradigm has raised questions that sound comical and intellectually bankrupt if asked in a different context.58 Steingraber’s departure from the dominant paradigm of cancer research is theoretically and practically important: if cancer is understood as a symptom of historically specific industrial practices and a lack of regulatory infrastructure, the terrain of preventive measures shifts dramatically. More important, for Steingraber and other activists, the types of prevention that become thinkable within the public health framework they advocate for also stand the greatest chance of significantly lowering the incidence of cancer—a reduction that has remained elusive despite the spending of over $100 billion since the war on cancer was declared, well over forty years ago.59 Cancer rate data and epidemiological research together support the thesis that a significant percentage of cancers with rising incidence rates are caused by carcinogenic toxins in the environment. A look at the types of cancers with the highest rates of increase (and, in some cases, mortality) reveals a strong correlation with the widespread use of industrial and agricultural chemicals that began after World War II.60 Cancers of the fatty tissues exhibit higher incidence rates than others, a phenomenon that may be explained by the fact that many of the chemicals introduced into the environment over the last fifty years tend to accumulate in the brain, breast, lymph nodes, bone marrow, and liver.61 Of the more than 200,000 breast cancer cases diagnosed annually in the United States, only an estimated 50 percent can be attributed to wellestablished risk factors such as reproductive history. This perplexing statistic has prompted reformers to call breast cancer an environmental disease, thereby making it an appropriate object of public health discourse. Indeed, there are several registers of evidence suggesting various environments are to blame: breast cancer rates vary according to geography and occupation, and they have been rising steadily—lifetime risk has nearly tripled over the last five decades, a rise that cannot be explained by the increase in mammography rates. Furthermore, women who immigrate to the United States have a greater risk for breast cancer than if they had remained in their countries of origin.

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Appropriating the language of Rachel Carson in an accompanying article titled “Pesticide Residues and Breast Cancer: The Harvest of a Silent Spring?,” David Hunter and Karl Kelsey wrote that, given the age-adjusted rise in breast cancer, “it is somewhat surprising that few investigators have examined the relationship between pesticide exposure and breast cancer.”70 The findings of Wolff ’s team were given added weight in 1994, when Eric Dewailly and coauthors published their conclusion that women with estrogen-positive tumors had a higher body burden of DDE than women with estrogen-negative tumors, suggesting that certain types of breast cancer may be triggered by DDT exposure.71 Three years later, Dewailly’s team’s investigation of the link between OCC exposure and estrogensensitive breast tumors prompted them to conclude that “the increase in estrogen receptor level in breast tumors observed during the past two decades could be explained in part by organochlorine exposure. If this hypothesis is confirmed, further limitations on production and usage of these chemicals will need to be implemented world-wide.”72 In a 1998 study of the pesticide dieldrin, researchers found that women with the highest traces of the pesticide were twice as likely to develop breast cancer as women with the lowest.73 And more recent research suggests that age at exposure could be relevant: one study found that exposure at an early age to significant amounts of DDT is associated with increased risk of breast cancer later in life.74 At the same time as these studies established sound hypotheses regarding the connection between pollution and breast cancer, the identification of the BRCA genes was garnering an equal, if not greater amount of public notice.75 After these genes had been sequenced and their contribution to breast cancer elucidated, it was not long before attention turned to “low” penetrance, more common genetic variants that contribute to breast cancer incidence.76 With knowledge of these alleles, genomics could play a greater role in breast cancer prevention, in particular by parsing out the complex etiology of a cancer that afflicts nearly 200,000 women each year.77 Making the case for the potential public health relevance of breast cancer genomics, one article noted: “The number of cases of breast cancer that are attributable to such genetic polymorphisms (in combination with environmental exposures) is likely to be much higher than the number of hereditary cases caused by mutations of high-penetrance genes such as BRCA1 and p53.78 The genetic polymorphisms that may be linked to breast cancer are much more common in the population than are the high-penetrance cancer susceptibility genes.”79

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reported reduced DNA repair capacity in family members of breast cancer cases, suggesting a potential genetic contribution to radiation sensitivity.87

Repair gene research thus provided a method of extending genomics research and explaining a much larger proportion of breast cancer cases.88 Indeed, “The most rapidly growing research area is now focusing on the association between DNA repair genotype and phenotypes in human cancer susceptibility.”89 The relationship between DNA repair SNPs and breast cancer risk has been a growing area of study.90 There are many reasons why repair gene research should be regarded as a positive development in both the prevention and treatment of breast cancer. In terms of prevention, the types of assays developed by repair gene researchers can verify an individual’s susceptibility to environmental mutagens well before damage has occurred. This is especially important for people for whom low levels of exposure are especially toxic. Repair gene research promises to shed light on the toxic effects of low exposures—not just to radiation, but also to other known or suspected carcinogens, such as environmental estrogens.91 Extreme susceptibility to a particular carcinogen should warrant special protections at the workplace or home, as well as heightened surveillance. And as I observed earlier, understanding the mechanisms of carcinogenicity helps environmental health advocates’ calls for stronger regulation of industry. Although the links between breast cancer and other toxins are not as well understood as that between the cancer and radiation, research regarding the latter has provided the evidence needed for environmental breast cancer groups to say that breast cancer is undoubtedly an environmental disease.92 Repair gene research also contributes to breast cancer research in that knowledge of sensitivity to IR is crucial for women who are diagnosed with breast cancer and are considering radiation therapy as part of their treatment.93 And such research may allow cancer doctors to develop interventions that will halt the proliferation of cancer cells by sensitizing them to radiationbased treatment. Simply put, by understanding how cells do or do not repair environmentally induced damage, cancer specialists could develop ways to target tumor cells and render them vulnerable to therapeutic interventions.94 Nevertheless, repair gene research invokes a model of gene-environment interaction that I argued earlier in the chapter is implicitly a privatized, market-based approach to public health. A guiding assumption of

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genetic susceptibility probably modifies their contribution at the individual level.”98 Exposures thus become meaningful (that is, actionable) only when individual responses to them are known; the ethical course of action is then modification of that person’s environment. “One of the most important problems in preventing and controlling breast cancer,” Hu and coauthors continue, “is the appropriate identification of high-risk individuals. Epidemiologic studies characterizing the molecular mechanisms of breast cancer risk are needed to further motivate genetically susceptible (sub)populations to get screened for early detection and intervention.”99 Environmental risk factors that are “amenable to intervention”100 include diet and the ill-defined yet popular risk factor of lifestyle, which connotes both a privatization of risk and the neoliberal, consumer-culture values on which it depends. The agent of disease—or, to put it another way, the agent of pollution— is the mutated gene or set of interrelated genes, not the industrial source of pollution. As a consequence, the agent of change is the individual harboring the genetic mutation, acting in concert with her physician. Mutations bear a historical narrative of evolution, making it difficult to see and comprehend the social situatedness of the woman with, or at risk for, breast cancer—put another way, her social location at the intersection of gender, race, and class. This model of environmental health is intelligible only insofar as the gene occupies a privileged status of actionable knowledge, despite the inherent ambiguity of a genetic test. What if, for example, other genes or other biological factors are at play that may determine one’s risk, factors that the test cannot reveal? Although understanding gene-environment interaction in the mechanism of disease is a laudable objective, it is a much more complicated process than genetic testing for susceptibility can speak to. The genetic test, as described by these researchers (and the directors of environmental genomics programs), presumably provides definitive evidence of inherited risk, evidence that can then inform and guide a set of individualized actions, which are, paradoxically, constrained by the immutable mark of heredity. To assume that a genetic test can and should set into motion one’s modification of the personal environment is to embrace a reductionist thinking that is belied by the post-HGP revelation that human biology is much too complicated for any theory of DNA or genes as immutable modifiers of environmental exposures—all the more so when one takes into consideration the synergistic effects of many lowpenetrance alleles.

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Estrogen metabolism also appears to vary according to race, with a higher ratio of inactive:active metabolites in whites compared to blacks. Thus, it appears possible that polymorphic variations in UGTs105 are one of the genetic factors accounting for these racial differences.106

Thus the racialization discourse analyzed in chapter 4 extends to the environmental health context as research shifts from improbable highpenetrance “founder” alleles of genes like BRCA1 and BRCA2 to low-penetrance genetic variations among women identifying themselves or being identified as black, African, or African American. Recall, though, that substantial evidence shows that social environments—themselves stratified by race and class—account for disease disparities (the likelihood of being diagnosed with premenopausal breast cancer is but one example). Chemical exposures as well as the experience of racism can alter biological processes, changes that can be mistaken as artifacts of heredity. Also as noted in chapter 4, socially induced stress can heighten the secretion of glucocortisoids, thus predisposing a woman to aggressive, premenopausal breast tumors. Moreover, environmental racism is another culprit in the ongoing investigation of health disparities in the United States. There is one noteworthy difference, however: whereas BRCA implicitly recast breast cancer disparities as hereditary phenomena for some black women (namely, young ones), polymorphism research, like that in the Carolina Breast Cancer Study, expands the heredity hypothesis to possibly include all black women. Although there is some chance that the epidemiological research exemplified by McClintock and others will resist geneticization, I have also argued throughout this chapter that this research, too, may be constrained by the power of proximate causes to capture the imaginations of doctors and public health officials. We may need a biosociality not only without genes, but without biology. In the next section, I explore this idea by discussing three areas of environmental health social movement: environmental justice, biomonitoring activism, and environmental breast cancer.

Race, Class, Gender, and the Embodiment of Pollution Environmental Justice Over thirty years in the making, the environmental justice movement has united its members around the shared experience of pollution. Notably, this movement does not rely or depend on elucidation of the biological

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petrochemical industry.111 Like other southern states, Louisiana is rich in natural resources (for example, its salt domes have been used for storing oil; brine, also plentiful, is necessary for the production of chlorine, which is used in the production of plastics)112 and is hostile to organized labor. In fact, the chemical industry increased production in Louisiana after it faced significant labor opposition in Texas in the 1950s.113 A study commissioned by Greenpeace in 1988 found that East Baton Rouge Parish had “more violators of emissions permits, commercial toxic waste facilities, employees in petrochemicals, and toxic waste generation than any other county along the [Mississippi] River, and, in addition, ranked second or third for 6 toxic emissions measures, 3 toxic discharges measures, and for toxic waste landfills and incinerators.”114 Geography alone does not fully explain these patterns—evidence surfaced in the mid-1980s that industry strategically targeted communities marked by poverty and political disenfranchisement.115 Industry also sought communities with documented antiregulation attitudes; it was effectively looking for communities with no history of economic justice social movements, itself a sign of political alienation. A 1984 study prepared by the consulting firm Cerrell Associates for the California Waste Management Board profiled neighborhoods most likely to successfully fight waste disposal sites. The study’s authors observed that “all socioeconomic groupings tend to resent nearby siting of major facilities, but middle and upper socioeconomic strata possess better resources to effectuate their opposition. Middle and higher socioeconomic strata neighborhoods should not fall within the one mile and five mile radius of the proposed site.”116 The Cerrell report became “the handbook for site location in the toxic-waste industry”117 and provided the following criteria for possible industrial development: residents should not be property owners; they should have a “free market orientation” and should not appear to favor a “socialist-welfare state”; and they should be employed by “nature exploitative occupations.”118 Industry counted on the political powerlessness of the mostly poor, African American population, virtually all of whom were deprived of the right to vote. By concentrating refineries and other factories in these communities, industry gained access to cheap land without worrying about political opposition.119 Once a site is chosen, the study concluded, industry should “decide, announce, defend.”120 The case of Convent, Louisiana, shows how devastating this pattern of industialization has been. In 2002 the population was 21,000 people, of whom 51 percent could not read or write, 61 percent were unemployed,

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included an exemption from local and parish property taxes for five years with a possible five-year extension, plus tax credits for each new job created—would amount to more than $94 million over ten years, an amount that would include $27 million in lost school tax revenue.132 Activists took this and other information to the community and beyond, going door to door, leading toxic tours, organizing letter-writing and petition campaigns, and holding town meetings. They also engaged in participatory research, gathering crucial demographic and epidemiological data. As a result, for the first time in the nation’s history, the EPA granted a suspension request due to suspected environmental racism.133 Before the EPA could finish its investigation, “the combination of protests, legal actions by Tulane’s law clinic and community groups, ongoing negative publicity, and the threat of a precedent-making federal action finally caused Shintech in September 1998 to withdraw its plan to build the plant at the Convent site.”134 Although the goal of the environmental justice movement in Lousiana and elsewhere has been the amelioration and prevention of pollution and disease in specific areas, its linkage with civil rights and economic justice has allowed it to demystify one of the more devastating ways in which institutional racism exacts its effects. These residents are not so much chemically exposed as they are chemically assaulted.135 This social movement has also provided the opportunity for coalition building136 and a vision of social transformation that includes long-term, primary prevention of environmental disease and its differential effects. Indeed, the obstacles faced by opposition groups and the successful siting of industrial facilities in the face of this opposition137 demonstrate the need for, at the very least, regional economic justice and political empowerment. For example, activists in Louisiana have struggled (not always successfully) to overcome state, municipal, and business support for chemical manufacturing as well as relentless attacks on their credibility by well-funded, influential elites.138 In 1998 the Louisiana Supreme Court ruled that, among other things, law students could no longer represent clients or groups affiliated with national organizations (the Tulane Environmental Law Clinic had provided pro bono assistance to activists), and that the majority of the students’ clients (75 percent) must satisfy the definition of “indigent.”139 Recalling a hearing during which one student lawyer defeated at least eight Shintech attorneys, the law clinic’s former director, Robert Kuehn, said: “The sad commentary is that the governor and the court are trying to say that eight licensed attorneys against one student attorney are not good enough

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the products we handle. The chemicals in question have been implicated in a variety of chronic diseases and reproductive disorders. In 2001 the CDC’s National Center for Environmental Health released its first “National Report on Human Exposure to Environmental Chemicals,” which made public, for the first time, data from the CDC’s National Biomonitoring Program. Interest in implementing biomonitoring programs since this first report has been substantial. In 2005 California enacted the country’s first statewide biomonitoring program—the California Environmental Contaminant Biomonitoring Project—and many other states are considering similar programs. Nonprofit organizations such as the Environmental Working Group have made biomonitoring studies central to their advocacy efforts, and community groups around the country have conducted biomonitoring studies as a way to raise awareness about the vulnerability of the human body to chemical exposures. These projects provide evidence of the ubiquity of chemical pollution, its unpredictable movement, and the permeability of body boundaries. Importantly, they need not be either disease-driven or dependent on the organic experience of suffering.145 They are epistemologically and ontologically significant because they provide material evidence of vulnerability; this newly perceived permeability of body boundaries reveals unforeseen connections or relations with other bodies in local, national, and even global contexts. Biomonitoring is a form of social action that can potentially effect significant policy and social change without recourse to knowledge of shared genes. And finally, it shows how progressive change can be realized within a particular milieu—in this case, “risk society.”146 Among the many features of risk society, according to Ulrich Beck’s landmark study, is the nature of risk itself. Some of the most pressing environmental risks we face, Beck says, are largely undetectable—they have no taste, smell, or color.147 Second, risk is constructed: it does not exist prior to the discourse that constitutes it as such. It is a term lacking a referent, a term without a corresponding material object. Together, these features of risk have entailed a certain set of relations between the public, environment, and knowledge. Beck explains: Risks induce systematic and often irreversible harm, generally remain invisible, are based on causal interpretations, and thus initially only exist in terms of the (scientific or anti-scientific) knowledge about them. They can thus be changed, magnified, dramatized or minimized within knowledge, and to that extent they are particularly open

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sphere when environmental science writers call on them. Risk experts in many ways occupy important positions in the “professional-managerial class,”150 whose interests overlap those of the upper classes even if their scientized discourse mystifies this convergence.151 Indeed, the existence of shared interests is by no means transparent—experts seemingly do not side with industry or with citizens. They instead occupy an apparently objective, value-free middle ground from which they mediate controversy. But risk experts accomplish this by operating within what has been called the “deficit-model” of public knowledge and understanding of science152—a strategic, self-serving, and not altogether accurate construction of their audience.153 Risk assessment and cost-benefit analysis entail two fundamental assumptions that have been the source of contention among community activists and academics alike. First, they assume that the notion of “acceptable risk” is a value-free, objective determination. Critics of risk have countered that “acceptable” is inherently normative, generally reflecting industry interests only, masquerading as common sense. Second, and related to this, risk assessment and cost-benefit analysis assume that risk should be managed, not reduced or eliminated. However, “managing” risks misdirects public debate about risk away from the search for safer alternatives and prevention more generally. Biomonitoring projects are not necessarily immune from these criticisms. They do, after all, produce data that can be translated into familiar frameworks of risk assessment: a person may test positive for traces of a particular chemical, but that does not necessarily mean that researchers or physicians can say for certain whether those detectable traces pose any sort of health risk. Nevertheless, biomonitoring projects have the potential to disrupt dominant risk narratives, and in many ways they have already done so. Similar to environmental justice’s implicit critique of risk assessment—in particular, the latter’s reliance on scientifically ascertained causes and effects and the notion of “acceptable risk”—body burden data motivate both social movement organizing and policy reform regardless of whether research demonstrates a connection between detectable exposures and disease. Biomonitoring achieves this by changing the way we think about our relationship with industrial practices and the free market principles that largely govern them. Biomonitoring studies compel participants to experience pollution as embodied and, in so doing, connect our lived experience with the lived experience of others—and with the social structures responsible for its production. In part, this is because the data

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to be found, because all women have been involuntarily exposed to toxic pollutants and, once exposed, store chemical metabolites in the body’s fatty tissues—in this case, the breasts. The act of breast-feeding reveals the biologically complex and thoroughly gendered dimensions of body burden.158 Testing over the years has revealed both the permeability of body boundaries and the persistence of chemicals classified as organochlorines. Many synthetic chemicals bioaccumulate (become concentrated) in human breast milk, making it one of the most contaminated foods on the planet.159 Richard Jackson, former director of the National Center for Environmental Health at the CDC, expressed the concern that “if you compared the legally allowable levels of toxic chemicals in human milk, you would conclude that half the human milk in the United States would be unfit for sale under FDA [Food and Drug Administration] guidelines.”160 As I observed earlier in this chapter, one way in which a woman can rid her body of these pollutants is through breast-feeding, thus casting into sharp relief the ways in which women’s bodies are inextricably tied to others.161 And as Steingraber notes in Having Faith: An Ecologist’s Journey to Motherhood, breast-fed infants, not their mothers, are at the very top of the food chain, relying on milk containing the largest amounts of bioacculumated toxins.162 The body burden of chemical contaminants—its history, geography, and modes of exchange—casts gender in quite a different light than has been typical in scientific research on breast cancer.163 Consider the risk factors for breast cancer most likely to be recited in public and specialized discourses alike: reproductive history, ethnicity, and socioeconomic status, the latter two being more or less substitutes for reproductive history. In practice, all three understand gender as an identity bound up with reproduction and thus reducible to it. Contrary to this, the body burden data in environmental breast cancer research implicitly presumes gender to be a property of embodied existence. It thus cannot be reduced to reproduction but instead reflects, and in turn imputes meaning to, the experience of living as a gendered person within a particular set of social relations—themselves inextricably tied to specific modes of production. For example, environmental breast cancer research shows the importance of understanding disease rates regionally and historically. Although methodological limitations make it difficult to ascertain when an exposure took place, the route it took, and the amount of chemical involved (not to mention the synergistic effects of exposure to multiple chemical agents), this research nevertheless raises the novel question of the

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offered a satisfactory explanation.168 Experiential knowledge by residents challenged the assumptions of breast cancer researchers, and cancer maps revealed that breast cancer was also high in poor and working-class neighborhoods.169 Women attending support group meetings at Adelphi University, for example, were not disproportionately old, Jewish, or rich. As Balaban noted, “the women were getting younger compared to the previous years.”170 However, a second study by the CDC affirmed the state health department’s conclusion that breast cancer incidence could be explained by Long Island’s demographics. According to the CDC’s researchers, when risk factors such as reproductive history, socioeconomic status, and ethnicity were taken into account, the risk was not higher for Long Island residents.171 Activists continued to mobilize, challenging the notion that women’s ethnicity or income and profession should be studied without taking environmental variables into consideration. Their efforts led to the June 10, 1993, passage of the federal Public Law 103-43 and with it the creation of the Long Island Breast Cancer Study Project (LIBCSP), the mandate of which was to study “potential environmental and other risks contributing in [sic] the incidence of breast cancer in Nassau and Suffolk counties” and the two counties with the highest age-adjusted mortality rates for breast cancer during 1983–87, which were Schoharie County, in New York, and Tolland County, in Connecticut. In addition, the law directed that the study “shall include the use of a geographic system to evaluate the current and past exposure of individuals, including direct monitoring and cumulative estimates of exposure, from (1) contaminated drinking water; (2) sources of indoor and ambient air pollution, including emissions from aircraft; (3) electromagnetic fields; (4) pesticides, and other toxic chemicals; (5) hazardous and municipal waste; and (6) such other factors as the [National Cancer Institute] director determines to be appropriate.”172 Funded and coordinated by the National Cancer Institute (NCI) and the NIEHS, the LIBCSP included a variety of research projects: epidemiological studies, a breast and ovarian cancer registry, and laboratory research examining the biological mechanisms by which synthetic chemicals might cause breast cancer. At the time, the LIBCSP was described as “ground-breaking epidemiological research”173 with the “most power to look at the relationship” between breast cancer and toxic chemicals.174 In addition, the LIBCSP is a rare example of a research program resulting from an act of Congress (Congress generally provides funding for agencies like the NCI, not for specific projects). Lawmakers further deviated

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the burden of proof on manufacturers so that they must demonstrate the safety of synthetic chemicals before they enter the marketplace. The precautionary principle further calls for regulation of these chemicals to be based not on incontrovertible scientific evidence (recognizing that scientific “certainty” is a mere construct and rarely, if ever, realized), but on evidence strongly suggesting the potential of synthetic chemicals to significantly compromise human health.179 Moreover, as Maren Klawiter observes in her ethnographic study,180 some environmental breast cancer activists have been justifiably suspicious of science-driven activism—extending their suspicions even to the practice of participatory research. These activists have rightly questioned whether epidemiology can produce actionable evidence of risk, given the inherent uncertainty of epidemiological research and the ways in which science funded by industry (usually via trade associations) permits it to strategically employ arguments about risk to delay environmental regulation. Demands for environmental reform, these activists believe, should never be contingent on the work of epidemiologists, regardless of their intent. Controversy around the organochlorine hypothesis is just one important example of the need to tie arguments about environmental breast cancer prevention to justice and ethics, not science. Notably, several studies—including those of the LIBCSP—failed to confirm a link between exposure to organochlorines and breast cancer risk.181 Science journalists and researchers alike have used the doubt generated by these studies to argue against further research. In 1994, for example, the Journal of the National Cancer Institute published a letter to the editor from Stephen Sternberg, arguing that the results of a single study proved that breast cancer is not a public health issue. Nancy Krieger, the author of said study, later accused Sternberg of propagating antiscientific and anti–public health sentiment. (Krieger argued that the spirit of “science” is continuing inquiry, regardless of conflicting results.)182 This exchange, and others like it, relegated to the technical sphere, had little positive effect on public discourse about the organochlorine theory at the time. Evidence supporting the environmental breast cancer hypothesis continues to accumulate, granting it ever more credence. Nevertheless, I want to suggest here that the environmental breast cancer movement remains a strong, viable, and diverse voice for social and political reform not merely because scientific evidence lends credibility to its political demands, but because breast cancer has been rearticulated as the experience of embodied social relations. This shared experience in turn necessitates collective

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inscribed by the social. They are symbolic as much as they are material; indeed, how bodies “matter” is very much a product of discourse.2 No object of scientific investigation or medical intervention comes to us ready-made but is, rather, the product of interest-driven discourses. Chapter 3, for example, showed how the ovary is an important site wherein hereditary fate and (obligatory) reproductive desire converge. Genomics thus benefits from the ovary’s social and symbolic importance; but it also reaffirms the place of the ovary (and the women tied to it) in the social and economic order—the ovary becomes an extension of heredity, of its manifest materiality. It becomes, in reconfigured form, the source of a fixed gender identity. By linking together the oophorectomy crisis in gynecology, feminist and queer theory’s challenge to the conflation of gender and sex, and genomics’ creation of an exceptional case—the BRCA mutation carrier—chapter 3 showed the unique and perhaps unexpected way in which heredity performs important recuperative work beyond the geneticization of disease already well documented by critical studies of genomics. This book also explored how the dynamic and evolving knowledge claims of genomics intersect with culturally coded and inscribed bodily facticities in the case of race. Chapter 4 documented how genomics’ interest in the health disparities between white and black women is more than an elucidation of complex biological processes involving ancestry and its probable role in differential breast cancer etiology. It is, as I showed, an investment in the biological race concept that is, simultaneously, an investment in the implicit assumption that racism does not sufficiently explain these disparities. Race, according to genomics, is something one inherits but does not embody. The pathology of institutional racism is thereby hidden through the (pathologized) genomic body, which in turn is racialized through a series of rhetorical displacements. Contemporary genomics is thus recast in chapter 4 as a discourse very similar to eugenics and scientific racism, insofar as the diseased body is taken to be a product of nature rather than particular social environments. African American women are urged to take greater care of their personal health by submitting to genetic counseling and testing. This model of health disparities is quite different from, and perhaps comes at the cost of, due consideration of the radical implications of theories of health disparities around synchronic understandings of race—radical because they explicitly or implicitly call for significant social change. Likewise in chapter 5, I considered how the gene-environment model helps normalize the practices of industrial capitalism by introducing the

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The basic principles of bioethics—autonomy, beneficence, nonmalfeasance, and justice (which holds that no one should be denied access to medicine and good health)—limit the field of analysis to the interactions between a woman, her counselor, and her physician. Feminist bioethics scholars have criticized this limited focus because it essentially concedes that the material conditions that brought forth the interaction or exchange cannot or should not be objects of analysis.3 Moreover, conventional bioethics’ main principles do not attend to the complexity of people’s lives. Informed consent, for example, rests on a limited notion of autonomy, one that presumes that a woman can—or should—be entirely free from outside influences. Beneficence cannot account for changing meanings of “health” and “disease” brought forth by the genomics revolution in medicine. Is it, for example, always a good idea to promote health if by doing so we expose women to dangerous therapeutic treatments based on risk alone? Feminists have also expanded the notion of justice to include gender justice—for example, by drawing attention to the specific ways in which medical issues affect the everyday lives of women. My hope is that the analysis in this book will help answer many of the questions raised by both conventional and feminist bioethics: Do genetic testing and subsequent interventions like prophylactic surgery uphold the principles of nonmaleficence and beneficence? Have alternatives to genetic testing been pursued? Is genetic testing, as a technology, the product of particular sets of social relations, with its design and use overdetermined by values attached to those social relations? On what grounds do women resist, and what can we learn from their resistance?4 How can we problematize autonomy and choice and the subject positions they require? More important, in what ways is genomics discourse constitutive of the subject positions that women come to inhabit? How does the relationship between knowledge claims and interventions become intelligible? And how might we understand these interventions beyond the limited framework of the doctor-patient relationship? Addressing such questions requires an analysis of the cultural and social norms that are called on in genomics discourse to fashion medical subjects; how these subject positions serve particular kinds of recuperative, ideological work (especially concerning gender and race); and how interventions such as surgery, explanations of health disparities, and public health surveillance are both evidence of changes in biomedicine that affect women as patients and normative statements about the world in which they live.

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undetermined: biosociality has no inherent politics; according to Rose, biosociality is merely a social structure for the enactment of particular projects, such as the demand for research dollars and other resources to investigate genetic disorders. And sociologists have shown how disease communities can often expand the field of political action considerably.7 In a somewhat similar vein, Margrit Shildrick has called on feminists to recognize and embrace new possibilities of identity and connection brought on by bioscience and, in particular, genetics. Shildrick argues that explorations of the human genome have called into question many of our most sacred truths. Although institutions often succeed in recuperating the normative body (what Shildrick describes as an imposing of order on the disorder brought about by bioscience), they cannot entirely contain the new relational possibilities that emerge in the wake of genomics’ conceptual obliteration of essential identities. What it means to embody genomics will always exceed or be underdetermined by ideology. Shildrick notes that genomics has routinely destabilized subjectivity and identity; the genome, as it turns out, does not provide the basis for firm boundaries between human groups or between humans and nonhumans. Genomics forces us to continually question and negotiate what it means to be human, opening up new possibilities for the enactment of world-transforming kinship. She writes: The very real ethical questions posed by bioscience in general and genetics in particular arise in the context of both an attempted shutting down of disorderly options, and a proliferation of uncontainable transformations and unforeseen connections. Where genetics may always threaten new patterns of oppression, we might also see new and positive possibilities of fluidity and connection. In the face of such a dynamic, the ethical undertaking cannot be to impose the order of answers that will prevail unchallenged over time, but rather to abandon the desire for the solid ground where certain analytic categories and concepts are fixed in advance. In consequence, the search for resolution, even for settled attributions of right and wrong, is no longer the primary concern. The task, instead, is to refuse an illusory closure and to continually reopen the questions themselves.8

In this passage, Shildrick situates herself within a group of scholars attempting the very important work of rethinking the terms of ethical principles without recourse to the very categories they are trying to destabilize.

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articulate, judge, and act upon ourselves in part in the language of biomedicine. From official discourses of health promotion through narratives of the experience of disease and suffering in the mass media, to popular discourses on dieting and exercise, we see an increasing stress on personal reconstruction through acting on the body in the name of a fitness that is simultaneously corporeal and psychological. Exercise, diet, vitamins, tattoos, body piercing, drugs, cosmetic surgery, gender reassignment, organ transplantation: the corporeal existence and vitality of the self has become the privileged site of experiments with the self.9

These bodily practices are, arguably, available only to those with the privilege to exercise them. This raises the questions, then, of how and whether these practices of the self also constitute resistance to ideologies of health. Might practices of the self, so construed, also be mechanisms for social control and for imposing limits on membership in the polity? Let me return to the example of race to draw out this particular point in greater detail. Bioethics principles can help guide the administration of genetic tests, and critical approaches can add to this by considering the ways in which race, gender, and the intersection of the two must inform the application of these principles. For example, bioethics addresses whether tests are available to black women, whether genetic counseling is duly attentive and sensitive to their information and decision-making needs, and whether counselors and physicians are more or less likely to recommend radical interventions like prophylactic surgery. However, because bioethics must limit its framework of analysis to the doctor-physician relationship—even if it interrogates the material conditions that give rise to and structure this relationship—it must act on behalf of black women as a group of women defined in some way by their genes. It cannot, then, question the ethicality of the very creation of the racialized testing subject, and it cannot ask whether the social designation “African American” should justify an analysis of her genome. Indeed, it is the racialized testing subject itself that makes the bioethical query possible. And the principle of justice can act as a further impediment to exploring the ethicality of racial medicine. Because BRCA testing, for example, is readily available to middle-class white women, bioethicists are obliged to problematize the low rates of testing among African American women in the United States. Within the terms of discussion set by traditional or conventional bioethics, justice would be

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for integrating genomics into health disparities research did not exist, neither would its support in the African American research community.12 The example of social movement that I described at the end of chapter 5 shows how the body can be the center of different epistemologies and politics. Environmental justice activists, for example, do not claim that race explains why they get sick from chemical pollution; it explains, rather, why the pollution is there in the first place. Industrial capitalism and institutional racism—their historical shifts, their specific practices— together give meaning to “race.” As a term, it is meaningful only by way of a synchronic analysis of racist practices. These racist practices are possible because the notion of racial inferiority remains widespread—a phenomenon for which genomics is partly responsible. And even when a social movement is organized around a specific disease—as in the case of breast cancer or sickle cell anemia—there are, I think, fundamental differences between a disease community and a mutation community. To identify with another based on a disease diagnosis initially limits the range of actions to that disease. But in many circumstances, there are opportunities for expanding the meaning of that connection. Breast cancer activism eventually led to environmental breast cancer activism, opening up the possibility for women to consider their position not only within a biomedicalized disease regime but within social relations more broadly. Environmental breast cancer activists identify themselves both as members of a disease community—all sharing a diagnosis of breast cancer—and as gendered, raced, or classed subjects with a particular relationship to industrial capitalism and the political entities charged with containing its destruction. The subject identity connected to a disease community is, as a consequence, fluid and contingent. In contrast, the disease community comprising BRCA carriers does not permit similar fluidity in identity and connection. The mutation fixes one’s identity; it is not something that can be altered. It is an identity rooted in evolutionary history, not social history. Social movements thus politicize disease in a way that gene-based biosocial communities do not. In environmental social movement, the diseased body and the bodyat-risk are together evidence of the materiality of social relations. But importantly, the body is not the locus of action, as in the body practices of somatic ethics. The locus of action is, rather, at the level of social and economic policy. In this way, social movements directly challenge genomics and its investment in an atomistic worldview. The atomized society of industrial capitalism, says Richard Lewontin, is matched in genomics by a

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26. Lowe 1995. In this way, Lowe departs from the work of biosociality theorists

27.

28. 29. 30. 31. 32. 33. 34. 35. 36.

37. 38. 39. 40. 41. 42. 43. 44. 45.

like Rose (2007). There are, I believe, two problematic assumptions on which the biosociality concept rests: (1) that the somatic self is more or less a new development (when in fact women and people of color have long been forced to lead corporeal existences); and (2) that the somatic self can be deciphered and theorized independent of economic structure. I do not disagree with biosocial theorists like Rose that developments in biomedicine and in the culture at large have brought about a particular somatic subjectivity, only with whether this constitutes a break with past cultural logics. I explore this point more fully in chapter 6. This is another point of departure for Lowe (1995): he calls on the critic both to account for economic structure and to attend to the governing practices of particular systems of oppression that cannot be reduced to it. Hartmann 1997; Barrett 1997; Nicholson 1997. Lowe 1995, 109. Sunder Rajan 2006; Cooper 2008; Waldby and Cooper 2008. Rose 2006, 160–61. See Feenberg 1991 for a critical theory of technology perspective. Stevens 2008. Stabile 1992. Stabile 1995, 415. This is one way in which I part company with scholars like Rose who draw on Foucault to make the case for interpretations of health discourses that disavow any notion that biomedicine acts as an ideological state apparatus. My approach here is that Foucault is helpful in understanding the production of new subjectivities (in particular how work on the body replaces explicit ideological appeals), but that new subjectivities do not necessarily tell us about the working of dominant interests. I say more about this in the conclusion. Oyama, Griffeths, and Gray, 2001. See Nelkin and Lindee 1995 and van Dijck 1998 for an appraisal of popular representations of genes. I provide a more complicated reading of genomics in chapter 5, especially with regard to gene-environment interaction. Haraway 1989, 15. Happe 2000. Ohmann 1996. Butler 1990. Harding 2006, 82. See also Condit 1999a. This perhaps explains the somewhat surpring results of ethnographic work that has studied the attempt of scientists to disavow race in favor of other terms, employing different software programs to do so. See, for example, Fujimura and Rajagopalan 2011.

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poor relief, and sterilization—all topics with which the family studies deal” (1988, 30). The discovery of Mendelism in 1900 appeared to provide solid scientific evidence of the mechanism by which traits are passed down among generations, although researchers did not know exactly what the substance of heredity was. The concept of the gene would be hypothesized for the first time by Wilhelm Johannsen in 1909. The following excerpt from a 1913 issue of Cosmopolitan captures this enthusiasm: “The long controversy about the relative influence of heredity and environment has been settled for all time. We know now that the possibilities of any individual are determined before birth” (Goodhue 1913, 148). The laboratory opened in 1904 with funds from the Carnegie Institute in Washington, D.C., for the study of evolution. Between 1910 and 1918, Harriman gave half a million dollars to the ERO. John D. Rockefeller contributed an additional $20,000 a year for four years. Before the American Eugenics Society was founded, activity included the formation of local eugenics groups across the country: the Galton Society, which met at the American Museum of Natural History (New York); the Race Betterment Foundation, in Battle Creek, Michigan; and “eugenics education” societies in Chicago, St. Louis, Wisconsin, Minnesota, Utah, and California. See Kevles 1985, chapter 3. For a history of the progressive era, see Danbom 1987. Haller 1984, 5. Southern and Eastern Europeans were considered nonwhite and, thus, inferior. They were also blamed for widespread labor unrest and some of the more radical and militant labor activism. For a social history of the 1920s, see Dumenil 1995. The term “germ plasm” was a precursor of the word “gene.” Wiggam 1922, 647. Wiggam 1926, 25. Between 1907 and 1963, almost thirty years after the demise of the eugenics movement, thirty states had sterilization programs and over 60,000 persons were forced to undergo this surgery (Reilly 1987, 161). As of 1987 sterilization laws were still on the books in 23 states (ibid., 166). Kevles 1985. Ibid., 56. See Happe 2000. See Ohmann 1996 for a detailed look at hegemony theory and the professional and managerial class. See Happe 2000 for the application of Ohmann’s theory to the specific case of eugenics discourse in mass-circulation magazines of the early twentieth century. Frank 1922, 317. Wiley 1919, 167.

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since there was considerable interest, in the United Kingdom, both in traits such as feeble-mindedness and psychosis as single-gene recessive traits and in sterilization for preventing their transmission. In the United States, she notes, eugenic sterilizations continued beyond the 1930s. For a history of sterilization in the United States, see Reilly 1987. Kay 1993, 8-9. Ibid., 9. Ibid., 44. Ibid., 47. Quoted in ibid., 36. Ibid., 45. Olby 1974; 1990, 506. Olby 1990, 513–14. Watson and Crick 1953b. For a short biography of Rosalind Franklin, see Hubbard 2003. According to Hubbard’s research, Watson and Crick could have never put together the model of DNA had they not had access (unbeknown to her) to Franklin’s X-ray diffraction images of DNA. Watson and Crick 1953a, 966. For a social history of the “code” paradigm, see Kay 2000. Watson and Crick 1953a, 966. Kuhn 1970. Rabinow 1992. Keller 1992b. Kevles 1985, 209. This is according to Paul 1995. Kevles (1985) dates its founding to 1950. Kevles 1985, 223. Ibid., 231. Ludmerer 1972; Kevles 1985. Ludmerer 1972. Kevles 1985, 254. Neel held a joint appointment in the Medical School and the Laboratory of Vertebrate Biology at the University of Michigan beginning in the late 1940s. Pregnant women participated in the study in order to get special provisions during and after the US occupation of Japan. Midwives were compensated with money, and “it was also stressed to them what a unique contribution to the scientific knowledge of the entire world they were in a position to make” (Beatty 1991, 302). Research still continues under the Radiation Effects Research Foundation, a research collaboration between the United States and Japan. “Race of monsters seen” 1952. “Geneticist warns on radiation rise” 1954, 117. Ibid. Quoted in ibid.

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nevertheless criticize Lysenko for the dogmatic, (and, as it turns out, antiprogressive) appropriation of Lamarck for Soviet plant genetics and political economy more generally. 95. Levins and Lewontin 1985, 168–69. 96. For this, I rely principally on Chafe’s (1999) history of the period. 97. I define this in the section on eugenics above. 98. Chafe 1999, 138. 99. Ibid., 144. 100. Keller 1992a, 288–89. 101. Ibid., 289. 102. Lewontin 1991. 103. Ibid., 67. 104. Ibid., 64. 105. The HGP included sequencing the human genome, mapping genes, and sequencing the genomes of other organisms such as bacteria (Escherichia coli), yeast (Saccharomyces cerevisiae), fruit flies (Drosophila melanogaster), and worms (Caenorhabditis elegans). The project’s goals also included the development of research technologies (such as sequencing technologies), technology transfer, and programs for publishing and distributing research data. 106. Wade 2003. The original estimate was $3 billion. 107. For book-length histories, see Bishop and Waldholtz 1990; J. Davis 1990; Wingerson 1991; Lee 1991; R. Shapiro 1991; Wills 1991; Cook-Deegan 1994. 108. Mapping simply refers to locating a gene on a chromosome; sequencing is the word used to describe identifying the chemical make-up of the gene. 109. Kevles 1992, 18–19. 110. Kevles 1997, 274. 111. Kevles 1992, 19. 112. Kevles 1997, 272. 113. Quoted in Kevles 1992, 22. 114. Quoted in Gilbert 1987, 27, 33. 115. Kevles 1997, 275. 116. Ibid., 275–76. 117. Ibid., 277. 118. Kevles 1992, 1997; Cook-Deegan 1994; Fortun 1995. 119. Although both the NIH and DOE declared a shared interest in both sequencing and mapping, the DOE was principally in charge of developing new sequencing and analyzing techniques, using several of the national laboratories and working with members of the computer science and physics communities. The NIH was principally responsible for mapping and for creating public databases, and it had sole responsibility for mapping model organisms. Additionally, the NIH took principal responsibility for producing and circulating medical applications of genomic research.

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editor in Science urging reconsideration of the project (Kevles 1997, 286). In 1990 Rechsteiner and Davis, two of the more vocal critics, were both asked to testify at a Senate hearing convened by Domenici. Yet only one of the two actually testified, and by then eleven of the twelve journalists who had attended the hearing had already left: “It was indeed evident that Domenici (nor for that matter any of the other senators who had shown up the hearing that day) was not particularly interested in hearing and considering criticism of what had been a favored project of his for several years” (Fortun 1995, 390). But even in 1991, Wyngaarden conceded that “if you took a vote in the biological sciences on the project, it would lose overwhelmingly” (quoted in Kevles 1997, 286). 128. Restriction enzymes allow geneticists to “cut” sections of DNA from one cell and bind it to the DNA of another. 129. Krimsky 1982. See also S. Wright 1994. 130. Interestingly, according to the media studies scholar Rae Goodell (1986), the rDNA controversy was short-lived; it did not take long for leaders of the scientific community to close ranks and support unrestricted research in this area. This was largely accomplished by the demonization of critics in public by other scientists (in an about-face from previous willingness to debate the issue of regulation), embargoes on journalists attending genetics conferences that prevented them from consulting outside experts, and some researchers refusing to grant journalists interviews unless they promised not to quote critics in the same article. For an excellent rhetorical analysis of the hearings in Cambridge, Massachusetts on a proposed ban on rDNA research, see Waddell 1990. 131. R. Wright 1990. According to Fortun (1995, 415–17), Watson had to have known that Congress would demand some sort of ELSI program. Kevles notes: “Watson was not only undaunted in his commitment to ethics but also, it would appear, shrewd. His policy undoubtedly helped defuse anxieties about the prospect of a genome project indifferent to or unrestrained by ethical considerations” (1992, 35). As of 1999, of the 172 studies granted ELSI funds, 73 (42 percent) were on topics related to educating the public and health professionals, assessing attitudes about genetics, and counseling individuals facing the choice of undergoing genetic testing or those who, having already undergone tests, have to negotiate the psychological, cultural, and interpersonal significance of the test results. See Juengst 1996 for a criticism of the ELSI program and the overrepresentation of these topics. 132. Koshland 1989, 189. 133. Office of Technology Assessment 1988, 85. 134. Chafe 1999, 473. 135. Ibid. 136. Ibid., 474.

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151. Everyone inherits two copies each of both BRCA1 and BRCA2. 152. Linkage analysis entails linking a known marker (for example, a polymor-

phism) on the genome and a particular phenotype (disease expression). If a group of individuals with a disease test positive for a known marker, researchers can assume that the gene for that disease resides close to that marker. Thus, researchers can narrow their search for the gene to a particular chromosome and to a particular location on that chromosome. If a family member has breast cancer but does not inherit a marker (due to the recombination of chromosomes during reproduction), then it is assumed that the gene is not close to that marker, and researchers rule out that particular region of the chromosome. In the 1980s, linkage analysis was used to map the Huntington gene in 1983 and the cystic fibrosis gene in 1985. 153. Jeff Hall et al. 1990. 154. They wrote: “Mapping genes for familial breast cancer is important because alterations at the same loci may also be responsible for sporadic disease” (ibid., 1684). In 1995 researchers observed damage to BRCA genes in sporadic tumors, and a debate ensued regarding how to interpret these findings. According to Lawrence C. Brody (personal communication, December 2000), it was believed that although BRCA plays some sort of role in sporadic cancer, it does so by a different mechanism than that which is involved in mutations that are inherited. 155. Miki et al. 1994. Autosomal dominant trait pattern simply means that one has only to inherit one bad copy of the gene to be at increased risk of cancer (as opposed to a recessive trait, in which two copies of a mutation must be inherited). 156. Wooster et al. 1995; Narod et al. 1991. 157. “Penetrance” refers to the proportion of individuals of a particular genotype that expresses its phenotypic effect in a given environment. 158. The guidelines expand considerably the number of women for whom a mutation can be predicted and who therefore should be offered screening. See ACOG 2009. 159. Sanz et al. 2010. 160. “Polymorphism” denotes a variation of a gene that may or may not be pathogenic. For clarity, I use the words “polymorphism” and “variation” to denote alterations of genes that may be benign and “mutation” to denote alterations that are not. For a study that exemplifies this particular research trajectory, see T. Smith et al. 2008. 161. Examples include variations of genes that affect how the body metabolizes carcinogens and genes that can repair the damage of such agents. 162. F. Collins et al. 2003, 7. This “vision” for genomics is certainly ambitious and arguably overstates just what genomics research is capable of accomplishing—the effect of pressure on scientists like Francis Collins (then director of

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challenging. Nevertheless, the percentage of total breast and ovarian cancer caused by mutant BRCA1 alleles will soon be estimated, and individual mutation frequencies and penetrances may be established. This in turn may permit accurate genetic screening for predisposition to a common, deadly disease. Although such research represents an advance in medical and biological knowledge, it also raises numerous ethical and practical issues, both scientific and social, that must be addressed by the medical community” (Miki et al. 1994, 71). Although some writers have claimed that the “newness” of genomics explains the lack of critical review by journalists (Rick Weiss and Susan Okie, personal communication, December 2000), the decline of investigative journalism has been affecting science reporting for some time. Many newspapers rely on reports from other papers or simply run wire-service stories. Even science writers at larger papers (and presumably with more resources) tend to rely on the testimony of the authors of research reports and other geneticists likely to corroborate the views of the study’s authors. Moreover, press embargoes often limit the time available for writers to investigate stories, thus exacerbating the problem of relying on testimony from the authors of research reports or short lists of establishment experts that rarely change. 183. Painter 1994. 184. T. Friend 1994. 185. Maugh 1994b. 186. Rochelle 1994. 187. The HGP, for example, was often talked about in terms of tackling the massive amount of information in DNA. Metaphors regarding the search for BRCA1 were similar: “if the total genome was represented by the distance between Bangor, Maine, and Miami, Florida, the researchers had narrowed the location of the breast cancer gene to the greater New York City area” (Davies and White 1996, 100). 188. Cowley 1993. 189. Saltus 1994. 190. Ibid., referring to recommendations by experts at the Dana-Farber Cancer Institute. 191. The study initially garnering attention was Wolff et al. 1993. Krieger et al. (1994b) published results that failed to confirm a link between DDT, PCBs, and breast cancer. But Dewailly et al. (1994) confirmed the results of Wolff et al. I talk more about this research in chapter 5. 192. In the text of the article, the writer claims that the 1994 Krieger et al. study “seems to eliminate” DDT and PCBs as suspects in the historical rise of breast cancer (Maugh 1994a). Likewise, the Atlanta Journal- Constitution claimed the study found “no evidence” of a connection between the chemicals and breast cancer (Husted 1994). 193. Kolata 2002; “Breast cancer mythology on Long Island” 2002.

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206. Ibid. 207. One must also consider the extent to which bioethicists have a professional

interest in many of the solutions they offer. For example, they often identify the shortage of genetic counselors as a significant problem, and training more counselors would largely be the responsibility of bioethics departments. Thus, recognizing the ethical problems of genetic testing, while also arguing that tests should remain part of medical care, fulfills their responsibility to be watchdogs and guarantees the necessity of their services. For a critique of the profession of bioethics, see Elliott 2001.

Chapter 3 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22.

23. 24.

Queller 2008. Queller was also interviewed by National Public Radio and other outlets. Tuttle et al. 2009. See Happe 2006. Sunder Rajan 2006 makes a similar point. American Cancer Society 2005. National Cancer Institute 2011b. American Cancer Society 2012. Centers for Disease Control and Prevention 2006. M. Goodman et al. 2003, 2676. Gilda Radner, a victim of ovarian cancer, was a well-known American actor and comedian. Piver et al. 1993a. Piver et al. 1993b. The lifetime risk for women in the general population is 1.8 percent. See King et al. 2003, 643. Gallion and Park 1995. Piver et al. 1993a, 588. Narod et al. 1991. See also Jeff Hall et al. 1990. See, for example, H. Risch et al. 2001; Olopade and Artioli 2004. Haber 2002; Kinney et al. 2005, 2509. See, for example, Piver et al. 1993a. Seltzer et al. 1995, 493. Runowicz 1999. Burke et al. 1997, 1000. See, for example, Tobacman et al. 1982. The full name of this cancer is primary peritoneal carcinoma or papillary serous carcinoma of the peritoneum (PSCP). The peritoneum is the tissue that lines the abdominal wall and covers most of the organs in the abdomen. For an overview of theories as to why PSCP is a risk for some women, including BRCA carriers, see Eisen and Weber 1998. Kauff et al. 2002, 1613. Rebbeck et. al. 2002, 1621.

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42. Ibid., 412. 43. Moscucci 1990, 156. See also Thiery 1998, 243; Dally 1991; Sengoopta 2000.

44.

45. 46. 47. 48. 49.

50. 51. 52. 53. 54. 55. 56. 57. 58. 59.

60.

“Cyrrhosis” is an alternative spelling for “cirrhosis.” Presumably, in the case of ovaries as in the case of the liver, cyrrhosis was the term used to denote scarring of the tissue. In the United States, it became known as “Battey’s operation” (after Robert Battey of the state of Georgia); in England, it was “Tait’s operation” (after Lawson Tait of England) (Studd 2006b, 412; Moscucci 1990), although Alfred Hegar of Germany is also credited for performing the surgery in 1872. In 1872 Robert Battey “presented before the American Gynecological Society four indications for surgery: (1) when the absence of a uterus threatened a patient’s life; (2) when it was impossible to restore an obliterated uterine cavity or vaginal canal by surgical means; (3) in cases of uterine or ovarian insanity or epilepsy; (4) in cases in which monthly periods produced prolonged mental and physical suffering” (Morantz-Sanchez 1999, 95). The openness with which Battey defined appropriate conditions for surgery suggests that he was performing surgeries often “for a range of vague mental and physical symptoms” (ibid). Literally, ovary-induced mania. Excessively painful menstruation. Studd 2006b, 413. Ibid. Barker-Benfield 1976, 121. William Goodell, a professor at the University of Pennsylvania, advocated performing an oophorectomy on all insane women because he believed insanity was a heritable trait (Dally 1991). Quoted in Sengoopta 2000, 426. Chapter 2 discusses the topic of eugenics in greater depth. See Ehrenreich and English 1978. For general histories of women and feminism, see Freedman 2002; Evans 1989. Smith-Rosenberg and Rosenberg 1999, 115. Quoted in Barker-Benfield 1976, 88. Smith-Rosenberg and Rosenberg 1999, 111. Ehrenreich and English 1978, 145. Smith-Rosenberg and Rosenberg 1999, 112. Morantz-Sanchez 1999; Sengoopta 2000. Smith-Rosenberg and Rosenberg 1999, 113. Moscucci writes: “In the last quarter of the nineteenth century, as Britain embarked upon its most ambitious programme of colonial expansion, imperialism stood little chance of success without motherhood” (1990, 159). Resistance to ovariectomy is thus an early instance of the strategic appropriation of popularly held ideas about femininity and womanhood in order to bring about reform (in this case, medical reform). Historians have described

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had the same discussion in the Netherlands. At that time it was customary to remove the ovaries whenever a woman aged ≥45 years was operated on by a gynaecologist. We had a hard time convincing our teachers that ovaries at the time of the menopause, and for a length of time thereafter, were still a prized possession. The reasoning of our elders was that once the ovaries were removed, no grim disease such as ovarian cancer (a cancer that is almost always beyond control at the time of detection) could develop” (1997, 204). Runowicz 1999. See LeWine 2005; Olive 2005. Piver and Wong 1997, 206. Davy and Oehler 2006, 167. Ibid. The authors put it quite forcefully: “In the absence of a known BRCA1 or BRCA2 mutation, or a very strong family history of ovarian and/or breast cancer, even the most fanatic gynecological oncologist would not suggest to a woman with low risk factors that she have bilateral oophorectomy to decrease the possibility of ovarian cancer” (167). Of course, what is considered “fanatical” changes over time, as the history of prophylactic oohorectomy suggests. Piver and Wong 1997, 206. See also Studd 2006a. According to a 1999 ACOG practice bulletin, reoperation rates for women who undergo hysterectomy can be as high as 5 percent, with pain in the retained ovary being the most common reason (ACOG Committee on Practice Bulletins 1999, 195). Also, women who have a hysterectomy tend to be younger, and risks associated with surgery increase with age. Davy and Oehler qualify this: “Repeat operations on usually much older women have their technical difficulties and complications. Furthermore, the procedure creates significant stress and anxiety for the patient until the ovarian malignancy is excluded. Thus, many operations on postmenopausal ovaries could be avoided by oophorectomy at the time of hysterectomy” (2006, 168). Studd cites research on women with endometriosis, for whom reoperation rates can be as high as 40 percent (2006a, 165). Piver and Wong 1997, 205–6. Parker et al. 2005b. Armstrong et al. 2004. The 300,000 figure cited earlier does not distinguish between women with or without BRCA mutations. Parker et al. 2005b, 219. Ibid., 222. Ibid., 223. Menopause increases the risk for heart disease—hence the conclusion that women should retain their ovaries as long as possible. Nevertheless, much more research is needed to fully understand the function of postmenopausal ovaries. The study by Parker’s team seems to suggest that the risk for heart disease is even higher when menopause is surgically induced at a young age. Complicating this further are data released from the Women’s Health

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death. In other words, the women more likely to undergo oophorectomy are more likely to be predisposed to the several diseases observed in the study; therefore, oophorectomy is not necessarily the causal factor. The problem with this logic is that history shows that oophorectomy is overprescribed for reasons that have nothing to do with factors that may predispose women to get the surgery. 104. See Lindsey 2006 for interviews with several physicians. 105. ACOG Committee on Practice Bulletin 2008, 237. 106. Eisenberg 2006. 107. E. Martin 1987. 108. Hickey, Ambekar, and Hammond 2009, 139. 109. In its 1999 practice bulletin on prophylactic oophorectomy, ACOG rates the following recommendation “Level C,” meaning “based primarily on consensus and expert opinion”: “Prophylactic oophorectomy should be considered for select women at high risk of inherited ovarian cancer” (ACOG Committee on Practice Bulletins 1999, 197). By 2008 the recommnedation had changed to “Level B,” meaning “limited or inconsistent scientific evidence”: “Bilateral salpingo-oophorectomy should be offered to women with BRCA1 and BRCA2 mutations after completion of childbearing” (ACOG Committee on Practice Bulletins 2008, 237). 110. If the decision model is valid, wrote one critic, “the public health consequences would be major” (S. Shapiro 2006, 163). 111. Haber 2002, 1660. 112. Ibid. 113. S. Miller et al. 2005, 655. 114. A. Goodman and Houck 2001, 93. 115. Liede et al. 2002, 1570. 116. Colgan et al. 2001, n.p. Although the researchers relied on self-reports of family history—a potentially significant limitation of the study—the Cass et al. study (2003) and others like it nevertheless point to a tendency among cancer geneticists to delink BRCA-related cancers from cases associated with cancer syndromes. Other studies have shown just what some extrafamilial variables might be. For example, in 2001 a large study of women with ovarian cancer revealed that women with nonmucinous tumors (those that are poorly differentiated and much harder to treat) were significantly more likely to test positive for BRCA mutations; the researchers concluded that it is “reasonable to offer genetic testing to all women with invasive nonmucinous ovarian cancer” (H. Risch et al. 2001, 708). Ethnicity has also emerged as a marker for genetic risk. In one study of Jewish women with ovarian cancer, the researchers concluded that “in light of the high probability of BRCA mutations in Jewish patients with ovarian carcinoma, we currently discuss genetic testing with all newly diagnosed, Jewish patients with ovarian/peritoneal or fallopian

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molecular changes preceding tumor development and reversing their course, then genetics will contribute in very positive, significant ways to women’s health care. The point of this chapter is merely to describe what scientific practices have emerged in the meantime. 127. Several studies have suggested that because cancer is often detected at the time of prophylactic surgery, the procedure in effect functions as a screening method, thus overcoming the limits of existing screening technologies. 128. Kauff and Barakat 2004, 277. 129. Davy and Oehler 2006,167. 130. Van Nagell 1991, 91. 131. The Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial collected data from 2002 to 2008 for about 30,000 women undergoing screening such as CA-125 and transvaginal ultrasound. Early results published found that screening does detect early-stage ovarian cancer but also results in many false positives (Buys et al. 2005). 132. Of course, I am not suggesting conscious strategizing on the part of geneticists to use heredity for the same ends as gynecologists did in the 1800s, only that the ways in which women’s bodies are available for intervention have changed. 133. Even if one remains suspicious of the Parker model, the Rocca study nevertheless calls into question the practice of prophylactic surgery for premenopausal women—a finding that was not, apparently, as controversial. It can also be argued that the kind of defensiveness provoked by the Parker study is almost always a response to any challenge to medical dogma. Kuhn’s (1970) thesis on scientific change is relevant here. 134. Eisen and Weber 1998. 135. Liede et al. 2002, 1575. 136. Karlan 2004, 520. One researcher concluded that HRT merely negates the reduction in breast cancer risk that oophorectomy provides, but this claim is unlikely to be persuasive to women with breast-ovarian heredity syndrome. 137. Estrogen-only HRT has not been shown to increase risk for breast cancer. It is unclear why. 138. Kauff and Barakat 2004, 277–78. 139. Kauff et al. 2002. 140. Grann et al. 2002. 141. King et al. 2001. 142. Grann et al. 2002. 143. Cass et al. 2003. 144. Schrag, Kuntz, Garner, and Weeks 1997. 145. Rebbeck et al. 2002, 1621. 146. Ibid. 147. In 2006, 315,930 women died from heart disease; this represents one out

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cancer risk, see Krieger 1989. I discuss Krieger’s essay in greater detail later, when I analyze the relationship between race, reproduction, and cancer risk. In a related vein, see Fausto-Sterling’s 1985 work on how flawed assumptions about estrogen have negatively influenced biological research about women. 167. Rebbeck et al. 2002, 1620. 168. Conversely, a BRCA1 carrier may want to undergo oophorectomy sooner rather than later, as her diagnosis will probably occur earlier than diagnoses for women in the general population. 169. Cass et al. 2003. 170. Ibid., 2193. Further evidence of this comes from Olopade and Artioli: “Of interest is that there have been no events in the 124 women who had oophorectomy by age 35 years, which suggests that the timing of oophorectomy may be important” (2004, S7). 171. Kauff and Barakat 2004, 277. For research regarding the protective effect of multiple, early pregnancies for women at risk for BRCA-related breast cancer, see Marquis et al. 1995; Holt et al. 1996; Jensen et al. 1996. 172. Heffner 2004. 173. Aliyu et al. 2005. 174. Faludi (1991). Consider the cyclical pathologization of the single and/or working mother in US public discourse, most often featured in front-page exposés in magazines like Time and Newsweek. The association of mental illness with single life, or with what is known as “having it all” (that is, both working and having a family) is a feature of biopolitics that Faludi famously identified as a key part of the backlash against US women in the wake of the feminist movement. 175. In an effort to make up for the dearth of knowledge regarding health in the lesbian community (many epidemiological studies do not note sexual orientation, so, for example, no one knows whether incidence rates of breast cancer are higher or lower for lesbians than for heterosexual women), Suzanne Haynes of the National Cancer Institute reported that lesbians were at a much greater risk of breast cancer than heterosexual women. Haynes did not report on incidence of breast cancer, however. Her methodology entailed generalizing lesbian lifestyles and noting the degree to which risky behaviors were more typical among lesbians. Based on assumptions such as fewer pregnancies and greater alcohol consumption, Haynes announced that as many as one in three lesbians is at high risk. The report garnered significant news coverage, which at times used the imagery of “plague” (“Cancer danger for lesbians” 1993; Raeburn 1993; Selvin 1993). Many of the news reports failed to mention that more research was needed to study these presumed risk factors as well as determine actual incidence of breast cancer. A study led by Stephanie Roberts of Lyon-Martin Women’s Health Services in San Francisco found significant differences in some risk factors (S. Roberts et al. 1998). In terms of incidence, however, Roberts

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Fausto-Sterling arguably disarticulates the categories from mere reproduction with her notion of a continuum (2000a, 2000b). 181. A. Davis 1981; Solinger 2001; D. Roberts 1997a; P. Collins 2000. 182. D. Roberts 1997b; Solinger 2001. 183. Another result is differential practices of prenatal genetic counseling. Genetic counselors, for example, have admitted to being more likely to recommend abortion for carriers of the trait for sickle cell anemia, reasoning that the perceived inability by women who carry the gene to care for the child renders medical care futile (Rapp 1998). 184. D. Roberts 1997b; Reilly 1987. 185. D. Roberts 1997b. Norplant is no longer on the market, but it is an example of how insidiously sterilization can be achieved. 186. Mosher and Jones 2010. There are many reasons for this, including cultural influences (for example, women tend to adopt the types of birth control practices they are most familiar with), racist practices of physicians and family planning clinics that offer sterilization for blacks at rates far higher than for whites, financing that makes sterilization more affordable than other types of birth control, and the understandable desire of black women to have as little contact with the medical community as possible. 187. M. Goodman et al. 2003, 2684. 188. Ibid., 2618. 189. Parham et al. 1997, 816–17. 190. Randall and Armstrong 2003, 4203. 191. Palmer et al. 2003. 192. Krieger 1989. 193. Martin et al. 2012. Recall, too, that lower ovarian cancer rates are thought to be explained in part by higher rates of sterilization among African American women. 194. Olopade 2004; Armstrong et al. 2005; Lipkus, Iden, Terrenoire, and Feaganes 1999; Kinney et al. 2001; Thompson et al. 2002. 195. It is beyond the scope of this chapter to speculate about other reasons why blacks refuse testing, such as concerns over the trade-off between genomics and social and environmental justice. Researchers investigating attitudes toward testing and associated levels of uptake do not seem to allow for reasons other than culture and the lack of uniform, national safeguards to protect privacy and employment (research on cultural differences in attitudes does have merit, although it is always carried out by comparing blacks and whites, which results in gross generalizations about both groups). I am sympathetic with Dorothy Roberts’s (1997b) argument that blacks’ skepticism of genomics is just as likely to be rooted in concerns over social justice as it is in fear of the medical community or of medicine more generally. (Of course, given the persistence of racism in medicine, it is not at all unjustified for blacks to be

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believe in “race” is evidence that “people are more readily perceived as inferior by nature when they are already seen as oppressed” (106). Clinton, Blair, Collins, and Venter 2000. Several of the early BRCA family studies detected the 185delAG mutation. See, for example, Struewing et al. 1995b. The letters and numbers “185delAG” signify the exact alterations of base pairs, which in turn explain the improper functioning of the allele. Struewing et al. 1995a This raised a whole host of issues regarding informed consent; see Goldgar and Reilly 1995. Ibid. Ibid., 199. Struewing et al. 1997. These variations in risk are rarely mentioned in the popular media. See chapter 2. Keoun 1997, 8. Among the countries mentioned in this article are Norway (one mutation is common in the eastern part of the country and another in the west), Iceland, Russia, the Netherlands, and Finland; also mentioned are persons identified as Japanese, Swedish, Italian (specifically, from Tuscany), African American, and Scottish. “Caucasian” is not normally considered an “ethnic” category. The articles I studied for this chapter use the terms “race” and “ethnicity” interchangeably or simply say “race/ethnic.” It is typical for these authors to say at the beginning of the article that they are studying “race/ethnicity” and later name specific groups. But they do not then say which of those groups are ethnic groups and which are racial groups—it is up to the reader to infer the difference. I do not bring this up to suggest that shared linguistic conventions would improve matters; indeed, the fact that racialization occurs despite the impressive array of word choices appears to support my point that race is a field-invariant habit of mind or ideology. Gao et al. 1997, 1233. Ibid., 1234. Ibid., 1235. Ibid., 1236. Ibid. See also Gao et al. 2000a; Pal, Permuth-Wey, Holtje, and Sutphen 2004. Earlier studies were inconclusive as to whether or not BRCA mutations would be found to a significant degree among African American women tested. A study in 1998, for example, found no mutations among any of the black subjects (B. Newman et al. 1998). Gao et al. 1997, 1235. Ibid., 1233. Other examples of using rates to justify research include M. Hall and Olopade (2006, 2201). Medullary carcinoma is a particular kind of tumor. It typically begins in the milk ducts and tends to be clearly differentiated from surrounding healthy tissue.

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I brought up these studies, she corrected my interpretation that the studies imply that we should consider interventions at the policy level to ameliorate health disparities. According to her interpretation, it was not social isolation per se that had led to higher glucocortisoid levels, but the perception of social isolation, a highly individualized assessment of both cause and level of intervention. Shim writes: “Related to such [individualizing] practices is the assumption that characteristics of one’s social environment, as incorporated in the multifactorial model, are exogenous to the individual—that one’s circumstances are taken as a given, as if individuals were dropped into a set of conditions that are not socially constructed nor patterned. Modern epidemiology, despite growing efforts to develop more ecological models that acknowledge causation at multiple levels, remains, therefore, predominantly concerned with the identification of individual-level risk factors, earning it the label of ‘risk factor epidemiology’” (2002, 133). Chowkwanyun 2011, 254. Chowkwanyun offers an account of race similar to what Stevens calls a “synchronic” view. See Stevens 2008. Krieger 1999. Krieger 2001, 668. Punctuation errors in original. I discuss the work of these critics below in the chapter. Toniolo and Kato 1996. The Ashkenazi studies garnered considerable media attention, and various advocacy organizations voiced concern that the research implied Jewish women were genetically defective and, as a result, were at greater risk for breast cancer than other women. The Jewish Women’s Coalition on Breast Cancer was formed as a result. The researchers themselves made it a point to say that Jewish women are at no greater risk for breast cancer than women in the general population. In an interview with the Journal of the National Cancer Institute, for example, Lawrence Brody claimed there are no data to show that rates of breast cancer are higher among Jewish women (Nelson 1998). For an example of “Jewish” breast cancer gene talk, see “Ashkenazi Jewish women” 1995. Science writers and researchers alike invoked the Ashkenazi BRCA research to explain higher rates of breast cancer on Long Island, where epidemiologists have suspected the influence of environmental pollution (see, for example, Hotz 1995). When the Long Island Breast Cancer Study (which I will discuss in more detail in chapter 5) was in the planning stages, geneticists approached the lead researcher to see if the study could include testing the subjects for BRCA mutations (Marilee Gammon, personal communication, September 2000). This did not happen, largely because of logistical problems associated with genetics research such as genetic counseling (ibid.) (It is worth noting, too, that in the Long Island Breast Cancer Study report, the authors note that known risk factors, including genetic predisposition, do not explain

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Feldman, Lewontin, and King 2003, 374. Ibid. Braun 2002, 167. Feldman, Lewontin, and King 2003, 374. For the perspectivalism argument, see Keller 1992b. Epstein (2007), drawing on Duster (1990), makes this excellent point as well. Geneticists could take the population of New York City and find alleles that are more frequent than in populations defined by a different city. As Epstein points out, there just isn’t any monetary or other motivation for such projects. C. Clarke et al. 2003. Brawley 2003b, 14. Olopade et al. 2003, 238, 240. See also Panguluri et al. 1999; Kanaan et al. 2003. Repeated Medline and Google searches failed to reveal any titles with the words “white” or “Caucasian” and “BRCA.” See de la Hoya et al. 2002 for information regarding Spanish mutations. See also German Consortium for Hereditary Breast and Ovarian Cancer 2002. Although “white” is typically referred to as a race, white women are studied with much more nuance than black women, as I discuss below. Table 4 in Haffty et al. 2006 (135) lists many mutations of unknown significance in white subjects. John et al. 2007. M. Hall et al. 2009. The groups were: Ashkenazi Jewish, Central/Eastern European, Latin American/Caribbean, Near/Middle Eastern, and Western/ Northern European (2224). These categories—along with the presumably “racial” labels “African,” “Asian,” and “Native American”—are drawn from the test requisition form administered during a BRCA screening. M. Hall et al. 2009, 2229; John et al. 2007, 2874. In both articles, the authors remind the reader that black women are more likely to be diagnosed at a young age with certain types of tumors, profiles that point to inherited susceptibility as the culprit. When genomics studies are more specific in describing subjects with African ancestry—for instance, those that employ the label “Yoruba,” “Yoruba” seems to stand in for “African”—rather than complicate it (as in the case of the Hap Map project; see International HapMap Consortium 2005). And, more important, these studies are not about breast cancer. John et al. 2007; Haffty et al. 2009. The neologism “young breast cancer” emerged in 2009 to denote this racialized disease category. Weitzel et al. 2007, 1615. Ibid., 1620. Montagu 1964. For an excellent analysis of the United Nations document, arguing why it did not dispense with race, see Reardon 2004.

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groups, individuals can nevertheless be grouped racially if one looks closely enough at genetic markers that distinguish the said groups according to evolutionary migrations out of Africa. 103. Long and Kittles 2003. 104. Stevens 2008, 324. For the language of “unique” mutations, see Gao et al. 2000a. For the research on “German” mutations, see German Consortium for Hereditary Breast and Ovarian Cancer 2002. 105. Stevens 2002. 106. Jones and Chilton 2002. 107. C. Clarke et al. 2003. 108. Krieger 2002, 612. 109. Trock 1996, 12. 110. C. Clarke et al. 2003, 215. 111. Brawley 2003a, 8. 112. For background on the field, see Steven Epstein 2007. 113. Brawley 2002, 471. For a discussion of residual confounding, see Kaufman, Cooper, and McGee 1997. 114. Institute of Medicine 2001, 8. 115. Krieger 2001, 672. For political economy approaches, see Lewontin 1991, 46; See also Levins and Lewontin 1985. 116. Krieger 2001, 668. 117. Ibid., 672. 118. Ibid., 673. 119. Ibid. 120. Most of the funding comes from the National Institutes of Health, specifically, the National Cancer Institute, the NIEHS, the National Institute on Aging, and the Office of Behavioral and Social Sciences Research. 121. Centers for Population Health and Health Disparities 2007, 12. 122. Gehlert et al. 2008, 340. 123. Centers for Population Health and Health Disparities 2007, 36. 124. Ibid., 34. See also McClintock et al. 2005. 125. I say much more about this hypothesis in chapter 5. 126. The racial stratification of chemical exposures is well documented. In one 1977 study, levels of DDT in blacks were twice those in whites, and researchers were twice as likely to find traces of lindane in black tissue samples as in white ones (Kutz, Yobs, and Strassman 1977). 127. Wolff, Britton, and Wilson 2003, 294. 128. Millikan et al. 2000. 129. McGregor et al. 1977; Russo, Tay, and Russo 1982; Trock 1996; Wolff, Britton, and Wilson 2003. 130. Krieger 1989, 210.

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several studies suggest is dangerous and should not be ingested (although, presumably, alternatives are not tested either, giving the public a false sense of security). 5. Kuehn summarizes this: “Repeated studies have shown that people of color and low-income groups live disproportionately closer to sources of pollution and waste and have disproportionately greater exposure to toxic substances. An extensive analysis of the empirical evidence revealed that all but one of twenty-seven studies of the proximity of communities to waste facilities and toxic releases found disparities by race and income. Each of the ten studies of ambient air pollution found that communities of color and lower incomes were subject to greater amounts of air pollution than white or more affluent communities. All of the studies of exposures and health effects also documented racial and income disparities, finding, for example, higher rates of exposure to lead in black and poor children; racial and income disparities in the levels of pesticides in the blood and fat; and disproportionate exposure to high levels of toxins in fish” (1996, 118–19). Dowie provides additional specifics: “Studies completed between 1990–1995 have shown that almost 50 percent of all African-American infants tested for lead had levels higher than the CDC standard; [that, according to an EPA study in 1992,] 3 out of 4 toxic waste dumps that were not in compliance with federal regulations were located in black and Hispanic communities; that communities with hazardous waste incinerators comprise 89 percent more people of color than the national average; that at least 15 million African Americans live in communities with one or more ‘uncontrolled’ toxic-waste sites; that about half of all Asian Americans, Pacific Islanders, and Native Americans also live near toxic-waste sites; that more than 200 million tons of radioactive waste are located on Native American reservations; that the rate for cancers of the reproductive and sex organs among Navajo teenagers is 17 times the national rate; that every year 300,000 farm workers, mostly Hispanic, suffer from pesticide-related illnesses; that pollution-induced asthma among innercity African Americans is much higher than the average for whites and it kills five times as many blacks as whites; and that African-American male children are three times as likely to die of asthma than white male children” (1995, 145–46). 6. Bullard 1990, 8. 7. Bullard defines “disadvantage” as “poverty, occupations below management and professional levels, low rent, and a high concentration of black residents [due to residential segregation and discriminatory housing practices]” (ibid.). 8. Ibid., 20. 9. Levins and Lewontin 1985; Krieger 2001. For a social history of epidemiological theories and practices, see Krieger 2011. 10. In the candidate gene approach, which has historically been more

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state. In environmental science, exposure biomarkers are used to evaluate physical or chemical changes in response to a particular exposure. An example would be DNA alterations brought on from exposure to environmental toxins. For an excellent essay on the links between biomarker development and biomedicalization of disease, see Shostak 2010. U.S. Department of Health and Human Services (2006). See also Schwartz and Collins 2007. National Institute of Environmental Health Sciences 2008; National Institute for Environmental Health Sciences N.d. See, for example, Levins and Lewontin 1985. Keller 2000. Schwartz and Collins (2007) seem to suggest that gene therapy is unrealistic, especially given more plausible opportunities for modifying exposures. Ibid. For the discussion of how genomics can improve environmental regulations, see National Institute of Environmental Health Sciences 2000. No long-term damage was inflicted on the apple industry: “Within five years, in fact, growers’ profits were 50 percent higher than they had been at the time of the 60 Minutes broadcast” (Rampton and Stauber 2001, 27). Although losses were suffered, according to Rampton and Stauber, much of them were due to a glut on the market that preceded release of the National Resources Defense Council Alar study on which the 60 Minutes segment was based. For more information on the council’s report, and the argument that it reported on evidence already known to the EPA using standard, accepted methods of risk assessment, see Tesh 2000. Ibid., 28. Any attempt by government to regulate—whether to contain occupational or public health hazards or raise the minimum wage, for example—will be resisted, as it is the responsibility of corporations and industry to maximize profits. An easy solution, of course, is for government to provide resources to help industry transition to safer alternatives. To say that we need genetic testing because regulations are too costly is like saying that because some antipoverty programs do not work, we should instead explore the relationship between poverty and individuals’ genetic susceptibility. Lan et al. 2004. For example, in 2009 the Lan team screened for SNPs and determined that genetic variants explained differences in susceptibility to benzene hematotoxicity (toxicity in the blood; benzene is implicated in blood as well as bone marrow diseases). Another term that theorists find useful in describing the impact that genomics has on public health regulation is “geneticization” (Sharp and Barrett 2000; Willett 2002; Lippman 1991; Edlin, 1987), or, the growing importance placed by doctors, public health officials and researchers, and biologists on exploring the genetic basis of disease at the expense of exploring other causes: “Overly

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45. Writing about the ethical, social, and legal implications of the EGP, the bio-

46. 47. 48. 49.

50. 51. 52. 53.

54. 55.

56.

ethicists Sharp and Barrett write: “In part, [debates about the EGP] concern possible discriminatory uses of genetic information, but the more fundamental issue is how information on genetic risks will alter our views on personal responsibility for one’s health” (2000, 280). For work in critical public health, see Petersen and Lupton 1996. Douglas and Wildavsky 1983. Waldby 1996, 3. Public health scholars, following the work of Foucault, have documented the ways in which, in an age of public health and “risk,” our ways of being in the world have fundamentally shifted. Put another way, the demands of the ethical life have changed (see, for example, Petersen and Lupton 1996). I do not wholly disagree with this, although when it comes to race, I argue that it is important to study the ways in which racism results in different types of imperatives for citizen-subjects and in which lax environmental regulations exact disportionate effects on African Americans and other minority groups—with deadly results. I discuss these points further in the concluding chapter. Schwartz and Collins 2007; Weis et al. 2005. National Institute of Environmental Health Sciences 2008; Weis et al., 2005, 846. See Steven Epstein 2007 for an excellent history and critical analysis of what he calls the “inclusion paradigm.” My argument here is similar to Duster’s in Backdoor to Eugenics (1990), in which he discusses how associations between alleles and disease in socially defined racial groups become grounds for understanding such groups as members of biological races. Here I am suggesting that what happens is that disease groups are defined first by spatial location, which then becomes the ground for transforming these disease communities into racial groups. It is, then, a much more insidious process. Miranda and Dolinoy 2005, 226. For example, Miranda and Dolinoy (2005) assert that when researchers control for confounding variables such as income and housing, race still determines disproportionate blood lead levels. It is hard to fathom how one could control for all the non-hereditary reasons that might explain why race is correlated with elevated blood levels. Similar to the examples I discuss in chapter 4, we see a rush to proffer biological and implicitly racialized explanations of health disparities. Enforcement of regulations is another matter altogether, and one does not need genomics for that. Moreover, body burden testing can be used—as it has already been—to determine whether lead regulations are working. And finally, it is worth noting that Herbert Needleman, whose use of tooth and blood

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with humans and wildlife has the capacity to mimic or obstruct hormone function—not simply disrupting the endocrine system like foreign matter in a watchworks but fooling it into accepting new instructions that distort the normal development of the organism” Krimsky 2000, 2). The environmental endocrine hypothesis casts significant doubt on key paradigms within the field of toxicology and the US regulatory structure that it informs. Specifically, because endocrine systems are homeostatic—that is, they operate according to self-regulated feedback systems—the general understanding among toxicologists that lower doses do not result in harmful effects has been cast into doubt (23). The environmental endocrine hypothesis, therefore, challenges toxicology’s inattention to the effects of low dosages on developing organisms and suggests that effects may even be “shut off ” if the dose is high enough (124). Estrogen is implicated in the proliferation of mammary cells, including tumor cells; it also plays a role in pregnancy-related risk because the differentiation of mammary cells, a byproduct of pregnancy, reduces risk. The manufacture of PCBs, which belong to the class of organochlorines, was banned in the United States in 1977, although controversy continues over how best to deal with their lingering presence in the environment. For an investigative study about PCB removal in the Hudson River in New York State, see Cray 2001. Allsopp et al. 1998. Wolff et al. 1993. See also Wassermann et al. 1976; Mussalo-Rauhamaa et al. 1990; Falck et al. 1992. Wolff et al. 1993, 652. Hunter and Kelsey 1993, 598. When considering cancer rates, it is important to adjust for age because rates are partially explained by aging populations (that is, cancer risk increases with age). Dewailly et al. 1994. Dewailly, Ayotte, and Dodin 1997, 888. Høyer et al. 1998. Cohn, Wolff, Cirillo, and Schultz 2007. See chapter 2. A. Martin and Weber 2000; National Cancer Institute 2012. S. Roberts et al. 1999, 785. As one team of researchers framed the issue, “it is estimated that about 5 percent of breast cancer cases are related to rare but highly penetrant genes, such as BRCA1 and BRCA. Because they are more common, however, low-penetrant cancer susceptibility genes in drug metabolism and DNA repair may contribute to a large proportion (> 90 percent) of breast cancer cases” (Hu et al. 2002, 208). It is noteworthy that of the dozens of articles on BRCA I have read, this gives by far the lowest estimate of the percentage of cases explained by the BRCA genes. The most common estimate is 5–10 percent; some estimates are higher. One essay on genetic repair limited

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93. The risk of cancer developing in the healthy breasts of patients was an early

motivating factor behind this research. 94. Khanna 2000, 800. See Jameel, Rao, Cawkwell, and. Drew 2004 for a review of

the literature on radiotherapy and radioresistance. 95. Hu et al. 2002, 208. The genes in question are the XRCC1, XRCC3, and APE1

genes. 96. Medina et al. (2002) employ the term “genomic instability” to describe this

inborn condition. 97. Hu et al. 2002, 209. 98. Ibid. 99. Ibid., 208. 100. Ibid., 213. 101. McClintock et al. 2005. 102. Hu et al. 2002, 213. See also Smith et al. 2008. 103. Guillemette, Millikan, Newman, and Housman 2000. The Carolina Breast

Cancer Study, started in 1993 (and now recruiting subjects for phase 3) examines disparities between African Americans and whites. Women are interviewed, their medical records assessed, and they provide a DNA sample. The UGT1A1 is not a repair gene, but it produces an enzyme that modifies the metabolism of estrogen—typically endogenous estrogen, but perhaps also estrogenic chemicals like those found in plastics and pesticides. Thus, its actual role in breast cancer susceptibility is different from the role of a repair gene, but UGT1A1 has captured researchers’ interest for reasons similar to those of the repair genes: to find susceptibility alleles that are low penetrant, yet widely dispersed (more prevalent) in specific populations. 104. See Kahn 2004 for a devastating critique of the rationale behind the Food and Drug Administration’s approval to market the heart medication Bidil to African Americans. 105. UGT genes are involved in the making of enzymes that are in turn involved in metabolism (for example, metabolism of carcinogens). 106. Guillemette, Millikan, Newman, and Housman 2000, 955. 107. Other factors, such as gender, certainly play a role in environmental justice politics; for now, however, I am focusing on race and class. Below in the chapter I address the topic of gender justice in the context of environmental breast cancer activism. 108. See Dowie 1995, 142. 109. See ibid. 110. See ibid., 143. 111. Markowitz and Rosner 2002. Louisiana’s relationship with the petrochemicalindustry dates back to the early twentieth century; it is home to oil wells, refineries, and offshore drilling (ibid., 234–40): “By the mid-1950s, chemicals

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remains unskilled (West and Melancon 2002). Bullard notes: “Even with the economic transformation, many of the region’s old problems that were related to underdevelopment (e.g., poor education, large concentrations of unskilled labor, low wages, high unemployment, etc.) went unabated” (1990, 32–33). 132. Markowitz and Rosner 2002, 272–73. 133. Ibid., 277–78. For an excellent study of toxic tours, see Pezzullo 2007. 134. Markowitz and Rosner 2002, 284. 135. For the language of chemical assault, see Bullard 2002. 136. Sandler and Pezzullo 2007; P. Brown 2007. 137. After deciding not to pursue its plans for construction in Convent, Shintech won approval to build a plant on a site across the river. Shintech avoided charges of environmental racism because no one lived at the new site—the entire community had been relocated by Dow in 1991 (Markowitz and Rosner 2002, 285). 138. One of the main lines of attack involved characterizing activists as dupes and puppets of the local and national organizations with which they were allied, including the Louisiana Environmental Action Network, Greenpeace, and Tulane Law School’s Environmental Law Clinic. The president of the Louisiana Association of Business and Industry publicly claimed that the civil rights argument was just a misguided attempt to revitalize a defunct movement: “Environmental justice is largely the creation of activists who turned to civil rights when environmental doom-saying no longer yielded results” (quoted in J. Roberts and Toffolon-Weiss 2001, 192). The governor weighed in eventually, attacking the clinic publicly; the secretary of the Louisiana Department of Economic Development attacked and attempted to discredit law clinic workers as elitists whose “agenda” undermined the chances of poor residents to obtain well-paying and secure employment (ibid., 113). 139. La. Sup. Ct. R. XX, full text available at http://www.lasc.org/rules/html/xx499. htm. 140. Quoted in J. Roberts and Toffolon-Weiss 2001, 202. Widespread resistance led to the watering down of these restrictions in 1999 (Markowitz and Rosner 2002, 281–82), but it is nevertheless the case that few of the clinic’s clients at the time would have been able to meet the new stipulations (J. Roberts and Toffolon-Weiss 2001, 202). 141. Quoted in J. Roberts and Toffolon-Weiss 2001, 201. 142. Proctor 1995. 143. Wagner 1995. 144. See P. Brown 1987 for a study of experiential knowledge and environmental health activism. Tesh complicates this in an interesting way, noting that a false dichotomy exists, in which activists are presumed to “feel” risks, while experts are presumed to “know” them (2000, 85).

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only intelligible to researchers and policymakers because of the bodily norms that ground our interpretive frameworks. Bodies are never abstract material objects—they are culturally gendered, sexed, and raced and, as such, are value laden and normative. Science and technology studies scholars working in the area of HIV/AIDS have shown that blood is never value free: its meaning is inflected with notions of risk and pathology attributed to the bodies from which it is drawn (Waldby and Mitchell 2006). Along these lines, Phaedra Pezzullo discussed the Environmental Working Group’s discourse of the “prepolluted” from a feminist perspective during a “Spotlight Scholar” talk she gave at the University of Georgia in April 2011. 155. Breast Cancer Fund and Commonweal, in a jointly produced document on the California bill, put it this way: “Just as individuals have a right to informed consent before undergoing medical procedures, we have a right to know what industrial chemicals are in our bodies that could be harmful to our health” (n.d., 1). They continued: “The presence of hundreds of industrial chemicals in the body does not mean it is ‘normal.’ Californians have not given permission to put untested chemicals in their bodies and we want to know more about what harm these chemicals may cause, what products contain these chemicals, and how people become exposed to them” ( 2). The authors of a Commonweal study observed: “When you hear the word ‘pollution,’ you think of polluted air, polluted water, polluted soil” (Patton and Baltz 2005, 3). Without a biomonitoring project, they argued, “Californians will continue to be part of a vast chemistry experiment” (8). 156. According to Davis Baltz of Commonweal, biomonitoring “is helping to create a revolution in our understanding of the links between exposure to chemicals and disease” (Patton and Baltz 2005). The cosponsor of the bill that established California’s biomonitoring program, Deborah Ortiz, claimed: “This law will help California create a strong, science-based program to establish links to chronic conditions, reduce exposure to toxic chemicals, and better protect our health and our environment” (Breast Cancer Fund 2006). 157. For excellent treatments of the environmental breast cancer movement and the science behind it, see Ley 2009 and McCormick 2010. 158. The first proposal for a statewide biomonitoring project in California would have made breast-milk testing the primary method of documenting body burden. 159. Steingraber 2001; Jackson 2000; Allsopp et al. 1998. 160. Jackson 2000, 7. 161. As Ley (2009) observes, activists have expanded their agenda to include children’s health, largely as a result of data concerning breast-milk contamination. 162. Steingraber 2001. For a multifaceted study of contaminated breast milk, see Boswell-Penc 2006. 163. See Steven Epstein 2007, chapter 11, for an excellent overview of the many

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and, 215, 215n176; mastectomy and, 88, 89, 214n162; non-BRCA genes and, 53, 202n167; oophorectomy and, 82–94, 213n133, 214n160; pollution and, 56, 148, 155, 158, 159, 204n197; pregnancy and, 215n176; privileging of African Ancestry and, 116–21; prophylactic oophorectomy and, 87–88; race and, 18–19, 96–97, 101–2, 107–11, 125, 128–30, 134, 160–61, 217n196, 218n1, 235n103; racism and, 134; radiation and, 156, 157, 235n93; religion and, 220n24; in white women, 96, 97, 107–8, 110, 119, 128–30, 134, 160–61, 223n69, 235n103. See also specific BRCA topics Breast cancer activists, 176, 187; education of, 56, 204n195, 204n197; growth pains of, 57, 204n201; media on, 56–57, 204n197. See also Environmental breast cancer activists Breast Cancer Fund, 154 Breast cancer research, 49, 58; on African American women, 109, 116–17, 220n23; on BRCA1, 54–55, 202n182; environmental genomics research and, 139–40; ethnicity in, 107; genetic variation in, 104; genomics and, 189n2; Long Island Breast Cancer Study, 172, 221n44, 240n164; oophorectomy and, 86–87; on populations, 104–5, 107, 110, 219n11; race in, 107; topics of, 204n204. See also Environmental breast cancer research Breast-feeding: body burden and, 171, 239n158; chemicals in, 171; environmental justice activism and, 239n161 Breast surgery, 89–90 Brown, Phil, 241n176 Bullard, Robert, 141, 227n7 Butler, Judith, 92–93, 216n180, 216n181 Cancer: age and, 233n70; causes, xiii; chemicals and, 153, 232n62; colon, xiii; environment and, 153; estrogen and, 90; genomics research, 18; health disparities in, 133; lifestyle and, 152–53; oophorectomy and estrogen-related, 76, 210n100;

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175–76; Long Island, 172–74, 240n164, 240n166 Environmental breast cancer research: body burden data in, 171; BRCA genes and, 56; on DDT, 56, 203nn191–92; gender and, 171, 239n163; Long Island Breast Cancer Study, 172, 221n44, 240n164; Long Island Breast Cancer Study Project, 173–74, 175; on PCBs, 56, 203nn191–92; regions in, 171–72 Environmental disease, 165 Environmental endocrine hypothesis, 154, 232n64 Environmental Genome Project (EGP), 144, 231n45 Environmental genomics: biosociality and, 150; breast cancer research and, 139–40; gene-environment model and, 150; new spatial and temporal dimensions to risk, 148–49; NIH and, 144; overview, 20–21, 139, 226n1; polluted body of, 152; pollution and, 145–46; risk privatization and, 140–52 Environmental Genomics Group, 145 Environmental justice, 164, 235n107, 236n129; class and, 235n107; gender and, 235n107; overview, 161–66; race and, 166, 187, 235n107 Environmental justice activism, 139, 140, 141, 237n144, 238n153; biomonitoring and, 167, 238n154; breast-feeding and, 239n161; critique of scientific expertise and, 166; embodiment perspective and, 162; industry and, 163–66, 236n131, 237n138, 237n140; in Louisiana, 163–66, 236n131, 237n138, 237n140; racism and, 166, 187; risk assessment and, 169, 238n153 Environmental justice movement, 139; environmental disease and, 165; pollution and, 161–62, 165 Environmental pollution. See Pollution Environmental Protection Agency (EPA), 139, 165, 168, 236n126 Environmental racism, 161, 162, 165, 166, 238n147

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Genetic repair: breast cancer and, 152–61; privatization of risk and, 157–59; racialization and, 160–61. See also Repair gene Genetic screening: of populations, 104–5. See also Genetic testing Genetics history: BRCA, genetic disease and post-HGP era, 49–59; DNA revolution and post-World War II U.S., 33–42; eugenics movement, 24–29; Human Genome Project and, 42–49; overview, 24 Genetics research: biochemical tests in, 30, 194n38; cancer treatment and, 212n127; eugenics and, 30; health disparities in, 137, 226n142; heredity in, 23, 38; reform eugenics and, 29–33. See also Human genetics research; Molecular biology research Genetic testing, 58; bioethics and, 59, 181, 205n207; black women and, 98, 185–86, 217n196; on chemicals, 147; environment and, 159; family history and, 79–80, 212n117; misuse of results, 230n36; ovarian cancer and, 212n117; race and, 98, 217n196; of white women, 98. See also BRCA testing Genetic variation: in breast cancer research, 104; public health and, 158 Genomics, xiii, 183; biology and, 48, 200n140; blacks and, 217n196; black women and, 217n196, 223n75; body and, 2–10, 177–79; breast cancer and, 155; breast cancer research and, 189n2; conceptual boundaries of, 160; diachronic view and, 6–7; discourse, 181; disease and, xv, 6, 143–44; environmental regulation and, 146; epidemiology and, 7; eugenics and, 4, 5; feminism and, 8, 18; founder mutations and, 116; gender and, 3, 6; gene-environment interaction and, 137; genetics compared to, 200n138; health disparities and, 116; hereditarianism and, xv, 5, 7; heredity and, xv, 5, 7–8, 10, 200n138; ideology and, 12–13; instability, 235n96;

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237nn137–38; science and, 166; women and industrialization, 20 Intersex, 93, 94, 216n181 Ionizing radiation (IR), 156 Jasanoff, Sheila, 5, 15 Jews: Ashkenazi, 104, 105, 109, 113–14, 221nn43–44, 240n165; BRCA mutations in, 109–10, 220n26; breast cancer in, 109–10, 113–14, 220n26, 221nn43–44; religion of, 109, 220n25 The Jukes (Dugdale), 25, 192n4 Kauff, Noah, 65, 83, 88 Kay, Lily, 31, 32 Keller, Evelyn Fox, 34–35, 41, 48, 49–50 Kevles, Daniel, 28, 31, 199n131 Khoury, Muin J., 143–44 King, Mary-Claire, 51 Klawiter, Maren, 175, 186 Krieger, Nancy, 97, 112, 129, 131, 132, 137, 175, 190n20, 214n167 Krimsky, Sheldon, 232n64 Kuehn, Robert, 227n5 Lamarckism, 23, 39, 196n94 Lead, 151–52, 231nn55–56 Lesbians, and breast cancer, 215n176 Levins, Richard, 39, 196n94 Lewontin, Richard, 39, 42, 122, 123, 126, 131, 187, 196n94 LIBCSP. See Long Island Breast Cancer Study Project Lifestyle: cancer and, 152–53; pollution and, 232n58 Linkage analysis, 51, 201n152 Long Island, and environmental breast cancer activists, 172–74, 240n164, 240n166 Long Island Breast Cancer Study, 172, 221n44, 240n164 Long Island Breast Cancer Study Project (LIBCSP), 173–74, 175 Louisiana, 163–66, 236n131, 237n138, 237n140 Lowe, Donald, 9, 191nn26–27

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compared to, 89–90; women in 19th century and, 69–71, 207n59. See also Oophorectomy Ovariotomy: gynecology and, 67–69; normal, 68–69, 207n44; overview and history of, 67–71, 206n28, 207n44 Parker, William, 74–76, 83, 210n95, 213n134 PCBs. See Polychlorinated biphenyls Penetrance, 224n83; of BRCA mutations, 51, 201n157; of genetic mutations, 122 Peritoneal carcinoma, 65, 205n22 Pesticides, 154–55. See also Chemicals; specific pesticides Petrochemical industry, 162–64, 235n111 Phenomenological perspective (of pollution), 140 Phenomenology (of pollution), 170 Politics: of biomedicine, 10–11, 14, 48; disease and, xiv; gender, 238n154; of genomics, 5, 6, 10; genomics, economy and, 3; of medicine, 189n10; naturenurture debate and, 41–42; race, history and, 128–34; of science, 5, 10, 14, 189n7; women and, 16, 192n51. See also Body politics Polluted body: class and, 161–70; environmental genomics and, 152; gender and, 170–76; genomics and, 139–76; race and, 161–70 Pollution: African Americans and, 162–64, 236n126; breast cancer and, 56, 148, 155, 158, 159, 204n197; cancer and, 153, 158, 164; class and, 162–66, 236n131; disease and, 143; environmental genomics and, 145–46; environmental justice movement and, 161–62, 165; as inevitable, 140; labor and, 162–63, 236n113; lifestyle and, 232n58; phenomenological perspective of, 140; phenomenology of, 170; race and, 141, 162–63, 227n5; socioeconomic status and, 163. See also Chemicals Polychlorinated biphenyls (PCBs), xiii, 141, 154, 233n66, 236n126;

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Rhetoric: culture and, 17; genomics and, 2, 17; heredity, disease and, 62, 80, 102; ideology and, 10–18, 40; progress, ideology and, 10–18; race and, 102–3, 107–14, 118, 120, 179; rhetorical construction of genetic risk, 178; rhetorical methodology, 14, 16, 17; rhetorical perspective of scientific discourse, 118; scientific objects as rhetorically constituted, 118 Ribonucleic acid (RNA): DNA and, 34, 39, 50, 196nn89–90; retroviruses, 196n90 Risch, Neil, 123, 124, 224n102 Risk: body burden data and, 170, 239n155; environmental, 149, 167–69, 230n44, 238n147; environmental genomics and privatization of, 140–52; experts, 168–69, 238n153; genetic repair and privatization of, 157–59; genomics and, 146, 148; rhetorical construction of genetic, 178; “risk society,” 167–68, 238n147 Risk assessment: biomonitoring and, 169–70, 238nn154–56; of chemicals, 148–49, 230n41; environmental, 168–69, 238n153; environmental justice activism and, 169, 238n153; of toxins, 148, 168 RNA. See Ribonucleic acid Roberts, Dorothy, 95, 217n196 Rockefeller Foundation, 31–33, 36 Rose, Nikolas, 10–11, 150, 183–86, 191n36 Rothenberg, Karen, 59 Rouse, Joseph, 189n7 Schwartz, David, 146, 149–51, 230n44 Science: bioscience, 183; class and, 14; culture and, 15; environmental racism and, 166; feminist science studies, 189n7; industry and, 166; liberal humanist view of, 58; media on, 58; politics of, 5, 10, 14, 189n7; public discourse about, 52–53; race and, 12, 135–37; rhetorical perspective of scientific discourse, 118; scientific objects as rhetorically constituted, 118 Science of Man project, 32 Screening: for BRCA mutations, 51, 201n158; BRCA testing compared to, 80–81; for

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in, 86, 213n148; industrialization and, 20; medicine and, 16, 192n51; mental illness and single, 215n175; ovaries and 19th century, 69–71, 207n59; politics and, 16, 192n51; pregnancy decisions of, 92; reproductive body and 19th century, 69–71, 207n59. See also Black women; Feminism; Gender; Motherhood; Pregnancy; White women Women’s Health Initiative, 74, 76 Xenoestrogens, 232n62

About the Author

Kelly E. Happe is an Assistant Professor in the Department of Communication Studies and the Institute for Women’s Studies at the University of Georgia.

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